Relevant bibliographies by topics / CD4 Receptors

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'CD4 Receptors'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "CD4 Receptors"

1

Ledbetter, JA, GL Schieven, VM Kuebelbeck, and FM Uckun. "Accessory receptors regulate coupling of the T-cell receptor complex to tyrosine kinase activation and mobilization of cytoplasmic calcium in T- lineage acute lymphoblastic leukemia." Blood 77, no. 6 (March 15, 1991): 1271–82. http://dx.doi.org/10.1182/blood.v77.6.1271.1271.

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Abstract T-lineage acute lymphoblastic leukemia (T-ALL) cells have abundant cytoplasmic CD3/Ti but express low amounts on the cell surface and are deficient in CD3/Ti-mediated signal transduction. Nevertheless, plating T-ALL cells on dishes containing immobilized anti-CD3 monoclonal antibodies with a source of growth factors induced the expression of CD25 (interleukin-2 receptor alpha chain) and stimulated the formation of blast colonies in 12 of 14 cases studied. The proliferative response to CD3 ligation was modulated by the presence of antibodies to the CD2, CD4, or CD8 accessory T-cell receptors. The effect of these accessory receptors on signal transduction mediated by CD3/Ti was next investigated by monitoring cytoplasmic calcium concentration [( Ca2+]i) and by measuring tyrosine phosphorylation after stimulation. Crosslinking CD3, CD2, CD4, or CD8 alone did not induce cytoplasmic calcium mobilization in T-ALLs, but crosslinking the accessory receptors with CD3/Ti induced calcium responses in three of the T-ALLs and enhanced calcium responses in three of the T-ALL cell lines, including HPB-ALL, MOLT-4, and CEM. Crosslinking CD4 but not CD2 with CD3/Ti greatly enhanced tyrosine phosphorylation of multiple substrates in comparison with crosslinking either CD4 or CD3/Ti separately on both normal mature T cells and the CEM T-ALL cell line. Thus, CD4 regulates CD3/Ti signal transduction in T-ALL cells through the tyrosine phosphorylation of substrates whereas CD2 may regulate [Ca2+]i signal transduction through a separate mechanism.
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2

Ledbetter, JA, GL Schieven, VM Kuebelbeck, and FM Uckun. "Accessory receptors regulate coupling of the T-cell receptor complex to tyrosine kinase activation and mobilization of cytoplasmic calcium in T- lineage acute lymphoblastic leukemia." Blood 77, no. 6 (March 15, 1991): 1271–82. http://dx.doi.org/10.1182/blood.v77.6.1271.bloodjournal7761271.

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T-lineage acute lymphoblastic leukemia (T-ALL) cells have abundant cytoplasmic CD3/Ti but express low amounts on the cell surface and are deficient in CD3/Ti-mediated signal transduction. Nevertheless, plating T-ALL cells on dishes containing immobilized anti-CD3 monoclonal antibodies with a source of growth factors induced the expression of CD25 (interleukin-2 receptor alpha chain) and stimulated the formation of blast colonies in 12 of 14 cases studied. The proliferative response to CD3 ligation was modulated by the presence of antibodies to the CD2, CD4, or CD8 accessory T-cell receptors. The effect of these accessory receptors on signal transduction mediated by CD3/Ti was next investigated by monitoring cytoplasmic calcium concentration [( Ca2+]i) and by measuring tyrosine phosphorylation after stimulation. Crosslinking CD3, CD2, CD4, or CD8 alone did not induce cytoplasmic calcium mobilization in T-ALLs, but crosslinking the accessory receptors with CD3/Ti induced calcium responses in three of the T-ALLs and enhanced calcium responses in three of the T-ALL cell lines, including HPB-ALL, MOLT-4, and CEM. Crosslinking CD4 but not CD2 with CD3/Ti greatly enhanced tyrosine phosphorylation of multiple substrates in comparison with crosslinking either CD4 or CD3/Ti separately on both normal mature T cells and the CEM T-ALL cell line. Thus, CD4 regulates CD3/Ti signal transduction in T-ALL cells through the tyrosine phosphorylation of substrates whereas CD2 may regulate [Ca2+]i signal transduction through a separate mechanism.
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3

Wee, S., G. L. Schieven, J. M. Kirihara, T. T. Tsu, J. A. Ledbetter, and A. Aruffo. "Tyrosine phosphorylation of CD6 by stimulation of CD3: augmentation by the CD4 and CD2 coreceptors." Journal of Experimental Medicine 177, no. 1 (January 1, 1993): 219–23. http://dx.doi.org/10.1084/jem.177.1.219.

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When T cells are activated via the T cell receptor (TCR) complex a number of cellular substrates, including some cell surface proteins, become phosphorylated on tyrosine (Tyr) residues. Phosphorylation of cytoplasmic Tyr renders these cell surface receptors competent to interact with proteins that link cell surface receptors to protein in the intracellular signaling pathways. Here we show that Tyr residues in the cytoplasmic domain of CD6 become phosphorylated upon T cell activation via the TCR complex. Tyr phosphorylation was observed when the T cells were activated by crosslinking CD3 or by cocrosslinking CD3 with CD2 or CD4, but not when the cells were stimulated by crosslinking CD2, CD4, or CD28 alone. Unlike other Tyr kinase substrates, such as the phospholipase C gamma 1-associated pp35/36 protein, whose level of Tyr phosphorylation is highest when T cells are activated by cocrosslinking CD3 with CD2, the levels of CD6 Tyr phosphorylation are highest when T cells were activated by cocrosslinking CD3 with CD4.
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4

Federmann, Birgit, Matthias Haegele, Christoph Faul, Wichard Vogel, Lothar Kanz, and Wolfgang A. Bethge. "Immune Reconstitution after Haploidentical Hematopoietic Cell Transplantation: Impact of Reduced Intensity Conditioning and CD3/CD19-Depleted Grafts." Blood 112, no. 11 (November 16, 2008): 1175. http://dx.doi.org/10.1182/blood.v112.11.1175.1175.

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Abstract Haploidentical hematopoietic cell transplantation (HHCT) using CD3/CD19 depleted grafts may lead to faster engraftment and immune reconstitution since grafts contain also graft-facilitating-cells, CD34− progenitors, NK cells, and dendritic cells. Reduced intensity conditioning may also have a positive impact on immune reconstitution following HHCT. 26 adults received CD3/CD19 depleted HHCT after RIC (150–200 mg/m2 fludarabine, 10mg/kg thiothepa, 120 mg/m2 melphalan and 5mg/day OKT-3 (day −5 to +14)) at our institution between 2005–2008. We prospectively evaluated engraftment and immune reconstitution. B-, NK-, T- and T-cell subsets (CD3/8, CD4/8, CD4/45RA/RO), TCR-Vβ repertoire and NK-cell receptors (NKP30, NKP44, NKP46, NKG2D, CD158a/b/e, CD85j, NKG2A, CD161) were analyzed by FACS. Grafts contained 8.8×106 CD34+ (range, 4.3–18.0 ×106), 2.9×104 CD3+ (range, 1.2–9.2×104) and 3.6×107 CD56+ (range, 0.02–23.0 ×107) cells/kg. Engraftment was rapid with a median time to >500 granulocytes/μl of 11 days (range, 9–15) and a median time to >20 000 platelets/μl of 11 days (range, 8–23). Full chimerism was reached on day 14 (median; range, 6–26). NK-cell engraftment was rapid, reaching normal values on day 20 (median of 247 CD16+CD56+CD3− cells/μl (range, 1–886)) with NK cells comprising up to 70% of lymphocytes. B-cell reconstitution was delayed with 81 (range, 0–280) and 335 (range, 11–452) CD19+20+ cells/μl on days 150 and 400, respectively. T-cell reconstitution was impaired with 49 (range, 0–586) and 364 (range, 35–536) CD3+ cells/μl on day 60 and day 150, respectively. We observed an increase of CD3+CD8+ cells in contrast to CD3+CD4+ cells early after HHCT with a median of 24 (range, 0–399) vs 16 (range, 0–257) and 159 (range, 1–402) vs 96 (range, 18–289) cells/μl on day 50 and day 200, respectively. CD4+CD45RA+ T cells increased slowly while CD4+CD45RO+ T cells reconstituted faster with a median of 61 CD4+CD45RO+ cells/μl (range, 0–310) vs 24 CD4+CD45RA+ (range, 0 to 152) on day 100. Within the CD4+CD25+ regulatory T cells there was a slow regeneration with median of 14 CD4+CD25+ cells/μl (range, 0–96) on day 100 and 28 CD4+CD25+ cells/μl (range, 19–160) on day 200. CD14+CD45+ monocytes did not reach normal values within the time of observation with 7 CD14+CD45+ cells/μl (range, 0–21) on day 120 and 7 CD14+CD45+ cells (range, 2–381) on day 400. TCR-Vβ repertoire and NK-cell receptor reconstitution was analyzed so far in 7 and 8 patients, respectively. We found a skewed T-cell repertoire with oligoclonal T-cell expansions to day 100 and normalization after day 200. An increased natural cytotoxicity receptor (NKP30, NKP44, NKP46) and NKG2A, but decreased NKG2D and KIR-expression was observed on NK-cells until day 100. In conclusion, T- and B-cell reconstitution is delayed after HHCT using CD3/CD19 depleted grafts and RIC. However, T-cell reconstitution is faster compared to data published with CD34 selected grafts and myeloablative conditioning. A fast NK-cell reconstitution early after HHCT was observed. Thus a combination of reduced intensity conditioning with CD3/CD19 depleted grafts appears to accelerate the immune recovery after haploidentical stem cell transplantation.
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5

Nikolova, Maria, Philippe Musette, Martine Bagot, Laurence Boumsell, and Armand Bensussan. "Engagement of ILT2/CD85j in Sézary syndrome cells inhibits their CD3/TCR signaling." Blood 100, no. 3 (August 1, 2002): 1019–25. http://dx.doi.org/10.1182/blood-2001-12-0303.

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Abstract Extensive phenotype analysis of cutaneous T-cell lymphoma (CTCL) malignant cell lines revealed surface expression of receptors usually not detected on normal circulating CD4+CD45RO+lymphocytes. We previously found that CTCL malignant cells express the killer cell immunoglobulinlike receptor (KIR) KIR3DL2/CD158k, whereas they fail to express the other KIRs. In the present study, we report for the first time that the CD85j/immunoglobulin (Ig)–like transcript 2 (ILT2) receptor is found on Sézary cell lines and on circulating Sézary malignant CD4+ cells, while it is hardly detectable on circulating CD4+ lymphocytes from healthy individuals. We demonstrate that ILT2 is functional on CTCL cells, as its triggering leads to the recruitment of Src homology 2 domain-containing tyrosine phosphatase (SHP-1) and to the specific inhibition of CTCL malignant cell proliferation induced by CD3/T-cell receptor (TCR) stimulation. Interestingly, we found that separated CD4+ILT2+ circulating malignant Sézary cells are less susceptible to anti-CD3 monoclonal antibody (mAb)–induced cell death than autologous CD4+ILT2− lymphocytes. Therefore, the resistance to apoptosis of Sézary cells may result from distinct mechanisms including cytokine-induced high levels of bcl-2 and specific expression of inhibitory receptors involved in lymphocyte survival.
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Forster, R., T. Emrich, E. Kremmer, and M. Lipp. "Expression of the G-protein--coupled receptor BLR1 defines mature, recirculating B cells and a subset of T-helper memory cells." Blood 84, no. 3 (August 1, 1994): 830–40. http://dx.doi.org/10.1182/blood.v84.3.830.bloodjournal843830.

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The G-protein-coupled receptor BLR1 related to receptors for chemokines and neuropeptides has been identified as the first lymphocyte-specific member of the gene family characterized by seven transmembrane-spanning regions. Using a high-affinity anti-BLR1 monoclonal antibody (MoAb) and three-color flow cytometry it is shown that BLR1 expression on peripheral blood cells is limited to B cells and to a subset of CD4+ (14%) and CD8+ (2%) lymphocytes. T cells expressing BLR1 were positive for CD45R0, were negative for interleukin-2 receptors, show high levels of CD44, and show low levels of L-selectin. The majority of CD4+ cells originating from secondary lymphatic tissue, but none of cord blood- derived T cells, express BLR1. These observations suggest that BLR1 is a marker for memory T cells. Furthermore, BLR1 expression was detected on all CD19+ peripheral or tonsillar B lymphocytes, but only on a fraction of cord blood cells and bone marrow cells expressing CD19, sIgM, or sIgD. Interestingly, activation of both mature B and T cells by CD40 MoAb and CD3 MoAb, respectively, led to complete downregulation of BLR1. These data suggest that the G-protein-coupled receptor BLR1 is involved in functional control of mature recirculating B cells and T- helper memory cells participating in cell migration and cell activation.
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7

Cayeux, S., S. Meuer, A. Pezzutto, M. Korbling, R. Haas, R. Schulz, and B. Dorken. "T-cell ontogeny after autologous bone marrow transplantation: failure to synthesize interleukin-2 (IL-2) and lack of CD2- and CD3-mediated proliferation by both CD4- and CD8+ cells even in the presence of exogeneous IL-2." Blood 74, no. 6 (November 1, 1989): 2270–77. http://dx.doi.org/10.1182/blood.v74.6.2270.2270.

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Abstract T cells generated during a second round of ontogeny after autologous bone marrow transplantation (ABMT) represent a unique model of early T- cell ontogeny in an autologous situation. Since grafted bone marrows were pretreated in vitro with the cyclophosphamide derivative ASTA Z 7557, circulating T cells had to be regenerated from reinfused hematopoietic progenitor cells. The T-cell population derived from 25 patients post-ABMT was phenotypically characterized: an increase in CD8+ cells, a low percentage of CD4+ cells, and a median of 12% CD56+ (NKH1+) cells were found. When the T cells were stimulated with phytohemagglutinin (PHA) and phorbol myristate acetate (PMA), defective interleukin-2 (IL-2) secretion was observed. In addition, proliferative responses of the T cells after activation through the antigen-receptor- dependent CD3 pathway, through the CD2 dependent alternative T-cell pathway, and by the lectin PHA were investigated. Despite the presence of CD2, CD3, alpha/beta chains of the T-cell receptor, and CD25+ IL-2 surface receptors, abnormal proliferative responses were obtained even in the presence of exogeneous IL-2. In experiments where the T-cell population was separated into CD4+ cells and CD8+ cells, both the CD4- and CD8+ subsets were unable to respond to activating and proliferating signals. Thus, T cells at early stages of ontogeny not only possess an intrinsic defect in IL-2 synthesis but, in addition, were unable to express functional IL-2 receptors in response to mitogenic stimuli.
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Cayeux, S., S. Meuer, A. Pezzutto, M. Korbling, R. Haas, R. Schulz, and B. Dorken. "T-cell ontogeny after autologous bone marrow transplantation: failure to synthesize interleukin-2 (IL-2) and lack of CD2- and CD3-mediated proliferation by both CD4- and CD8+ cells even in the presence of exogeneous IL-2." Blood 74, no. 6 (November 1, 1989): 2270–77. http://dx.doi.org/10.1182/blood.v74.6.2270.bloodjournal7462270.

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T cells generated during a second round of ontogeny after autologous bone marrow transplantation (ABMT) represent a unique model of early T- cell ontogeny in an autologous situation. Since grafted bone marrows were pretreated in vitro with the cyclophosphamide derivative ASTA Z 7557, circulating T cells had to be regenerated from reinfused hematopoietic progenitor cells. The T-cell population derived from 25 patients post-ABMT was phenotypically characterized: an increase in CD8+ cells, a low percentage of CD4+ cells, and a median of 12% CD56+ (NKH1+) cells were found. When the T cells were stimulated with phytohemagglutinin (PHA) and phorbol myristate acetate (PMA), defective interleukin-2 (IL-2) secretion was observed. In addition, proliferative responses of the T cells after activation through the antigen-receptor- dependent CD3 pathway, through the CD2 dependent alternative T-cell pathway, and by the lectin PHA were investigated. Despite the presence of CD2, CD3, alpha/beta chains of the T-cell receptor, and CD25+ IL-2 surface receptors, abnormal proliferative responses were obtained even in the presence of exogeneous IL-2. In experiments where the T-cell population was separated into CD4+ cells and CD8+ cells, both the CD4- and CD8+ subsets were unable to respond to activating and proliferating signals. Thus, T cells at early stages of ontogeny not only possess an intrinsic defect in IL-2 synthesis but, in addition, were unable to express functional IL-2 receptors in response to mitogenic stimuli.
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9

Signoret, N., M. M. Rosenkilde, P. J. Klasse, T. W. Schwartz, M. H. Malim, J. A. Hoxie, and M. Marsh. "Differential regulation of CXCR4 and CCR5 endocytosis." Journal of Cell Science 111, no. 18 (September 15, 1998): 2819–30. http://dx.doi.org/10.1242/jcs.111.18.2819.

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The chemokine receptors CCR5 and CXCR4 are major co-receptors/receptors for the CD4-dependent and CD4-independent entry of human and simian immunodeficiency viruses. The chemokines that bind and activate these receptors can inhibit the entry of viruses that use the respective co-receptor molecules. Chemokine-induced co-receptor internalisation is a significant component of the mechanism through which chemokines inhibit virus entry. CXCR4 internalisation is induced by the CXCR4 ligand stromal cell derived factor-1 (SDF-1), phorbol esters and, in T cells, cellular activation. Here we show that CXCR4 endocytosis can be mediated through either one of two distinct internalisation signals. A COOH-terminal serine rich domain is required for ligand- but not phorbol ester- induced CXCR4 internalisation. However, a Ser/IleLeu motif, similar to that required for the endocytosis of CD4 and the T cell receptor/CD3 complex, is required for phorbol ester-induced, but not ligand-induced, CXCR4 endocytosis. By contrast, CCR5 internalisation is induced by the beta-chemokine RANTES but not by phorbol esters. CCR5 lacks the Ser/IleLeu sequence required for phorbol ester-induced uptake of CXCR4. Together these results indicate that distinct mechanisms can regulate CXCR4 and CCR5 endocytosis and trafficking.
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10

Forster, R., T. Emrich, E. Kremmer, and M. Lipp. "Expression of the G-protein--coupled receptor BLR1 defines mature, recirculating B cells and a subset of T-helper memory cells." Blood 84, no. 3 (August 1, 1994): 830–40. http://dx.doi.org/10.1182/blood.v84.3.830.830.

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Abstract:
Abstract The G-protein-coupled receptor BLR1 related to receptors for chemokines and neuropeptides has been identified as the first lymphocyte-specific member of the gene family characterized by seven transmembrane-spanning regions. Using a high-affinity anti-BLR1 monoclonal antibody (MoAb) and three-color flow cytometry it is shown that BLR1 expression on peripheral blood cells is limited to B cells and to a subset of CD4+ (14%) and CD8+ (2%) lymphocytes. T cells expressing BLR1 were positive for CD45R0, were negative for interleukin-2 receptors, show high levels of CD44, and show low levels of L-selectin. The majority of CD4+ cells originating from secondary lymphatic tissue, but none of cord blood- derived T cells, express BLR1. These observations suggest that BLR1 is a marker for memory T cells. Furthermore, BLR1 expression was detected on all CD19+ peripheral or tonsillar B lymphocytes, but only on a fraction of cord blood cells and bone marrow cells expressing CD19, sIgM, or sIgD. Interestingly, activation of both mature B and T cells by CD40 MoAb and CD3 MoAb, respectively, led to complete downregulation of BLR1. These data suggest that the G-protein-coupled receptor BLR1 is involved in functional control of mature recirculating B cells and T- helper memory cells participating in cell migration and cell activation.
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Dissertations / Theses on the topic "CD4 Receptors"

1

Bernhard, Oliver Karl. "Proteomic Investigation of the HIV Receptors CD4 and DC-Sign/CD209." University of Sydney. Medicine, 2004. http://hdl.handle.net/2123/585.

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HIV infection and disease is a multistage process that involves a variety of cell types as the virus spreads through the body. Initially, dendritic cells (DCs) present at the mucosal site of infection bind and internalise HIV for degradation and presentation to T cells. As the DCs migrate to lymph nodes and mature, part of the internalised virions remains infective inside endosomal compartments. During formation of the immunological synapse between CD4 T cells and DCs, infective virions from dendritic cells are transferred to CD4 T cells leading to a strong infection of those cells allowing rapid virus dissemination throughout the body and establishment of the typical HIV infection. Various membrane receptors are involved in this process. Initial HIV binding to DCs is mediated by C-type lectin receptors such as the mannose receptor or DC-SIGN (DC specific intracellular adhesion molecule 3 grabbing non integrin) which is followed by virus internalisation and lysis albeit virus induced changes in endocytic routing prevents a proportion from degradation. Productive infection of DCs has also been observed allowing trans infection of CD4 T cells through a different mechanism. HIV infection of CD4 T cells, DCs and other cells is a multistep process initiated by binding of HIV envelope gp120 to the CD4 receptor, a 55 kDa transmembrane glycoprotein. Subsequent conformational changes in gp120 allow binding to a chemokine receptor, either CCR5 or CXCR4, followed by membrane fusion and infection. The aim of this thesis was to investigate protein associations with the HIV receptors DC-SIGN and CD4 in order to elucidate the mechanism of complex formation, virus entry and/or defining target sites for antiretroviral drugs. This thesis used a proteomic approach for studying the receptors with mass spectrometry-based protein identification as its core technology. A range of different approaches were developed and compared for identification of protein interactions and characterisation of the identified protein associations. An affinity purification of the CD4 receptor complex from lymphoid cells was used as the basis for detecting novel CD4-binding proteins. For this approach a strategy based on mass spectrometry identification of CD4 associating proteins using affinity chromatography and affinity-tag mediated purification of tryptic peptides was developed. This method proved successful for the identification of CD4 interacting proteins such as the strongly associated kinase p56lck, however a limited number of non-specifically bound proteins were also identified along the receptor complex. Using one-dimensional SDS-polyacrylamide gel electrophoresis followed by in-gel digests and mass spectrometry analysis, a large number of non-specifically binding proteins were identified along the CD4/lck complex. Evaluation of different lysis buffers in several independent experiments demonstrated that there was a large and inconsistent array of proteins that were obviously non-specifically bound to the receptor. No further specific binding partners were detected. These data suggested that protein interactions of CD4 on this cell type are of weak and/or transient nature. It also demonstrated a need for careful interpretation of proteomic data in the light of the propensity of non-specific binding under these conditions. To overcome dissociation of weak protein interactions, a method was developed using chemical cross-linking to preserve weak protein interactions on lymphoid cells. Affinity purification was used to purify CD4 along with cross-linked associated proteins and mass spectrometry analysis identified an interaction with the transferrin receptor CD71 and the tyrosine phosphatase CD45. The CD45-CD4 interaction is well known. The CD4-CD71 interaction was demonstrated to be a result from colocalization of the two molecules during formation of endocytic vesicles. Flow cytometry-based fluorescence resonance energy transfer (FRET) measurements were applied to confirm colocalization. A similar interaction was suspected for CD4 and DC-SIGN on the plasma membrane of DCs as cis infection of DCs has been demonstrated i.e. initial binding to DC-SIGN then to CD4/CCR5 on the same cell. Therefore, protein associations of DC-SIGN were investigated using the developed techniques. Using cross-linking, DC-SIGN was shown to assemble in large complexes on the surface of immature monocyte-derived DCs. Mass spectrometry analysis of the purified complexes identified them as homo-oligomers of DC-SIGN. The absence of CD4 suggested that the fraction interacting with CD4 at any one time must be small. The complexes of DC-SIGN were further characterised to be tetramers and successfully co-immunoprecipitated with HIV gp120 and mannan. DC-SIGN monomers were not evident demonstrating that the assembly of DC-SIGN into tetramers is required for high affinity binding of its natural and viral ligands. Thus potential antiviral agents aimed at blocking the early stage of HIV binding to DCs must simulate tetramers in order to neutralise the virus efficiently. Overall the thesis provides new information on protein interactions of CD4 and DC-SIGN, a careful investigation of "proteomics" techniques for identifying the proteins in affinity-purified samples and demonstrates the need for multifaceted analytical approaches to probe complex cellular systems.
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2

Sather, Blythe Duke. "CD4+ Foxp3+ regulatory T cell homing & homeostasis /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8343.

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Jacobs, Caron Adrienne. "The nanoscale organisation of HIV cell surface receptors CD4 and CCR5." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10056281/.

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The plasma membrane serves as the cell’s front line for interactions with, and response to, the external environment. The molecular mechanisms and regulation of cellular responses to extracellular signals are determined by the spatial organisation and dynamics of the various components comprising the plasma membrane. CD4 and CCR5 are two key cell surface molecules with important roles in immune cell function and regulation. They are also co-opted as the primary receptor and a co-receptor, respectively, by HIV. Biochemical studies have provided a detailed understanding of the molecular mechanisms of these interactions. Until recently, however, the small scale and rapid dynamics of these interactions has meant that a detailed view of the topology of the cell membrane and the organisation of receptors first encountered by the virus has been beyond the resolving power of available tools. The increasing capabilities of the emerging and rapidly developing super-resolution microscopy technologies are now optimally poised for us to address some of these questions. In this work, I have applied single molecule localization microscopy to unveil some of the nanoscale organisational properties of the cell surface receptors CD4 and CCR5. I have worked on the development of small labelling probes for CD4 and addressed some of the key aspects of sample preparation and labelling that can artificially alter the distribution of membrane associated target molecules. Here I report the first quantitative characterisation of the nanoscale organisation of CD4 and CCR5 in lymphoid cell plasma membranes, as well as how this organisation changes under different conditions, such as in response to cell signal-mimicking stimulation, or exposure to HIV envelope. This approach to characterising membrane receptor organisation can be further applied to in-depth studies of early host cell-virus interactions, as well as to other cell surface receptors and their organisation in the context of key cellular functions.
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Wong, Phillip. "Changing TCR recognition requirements at discrete stages of intrathymic CD4 T cell development /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8351.

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Sáez, Borderias Andrea. "Regulation of natural killer and cd4+T cell function by NKG2 C-type lectin-like receptors." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7133.

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This work is centered on the study of the NKG2 C-type lectin-like receptors on NK and CD4+T cells. We provide evidence supporting that CD4+T cells specific for Human Cytomegalovirus (HCMV) may express different NK cell receptors, and demonstrate that the C-type lectin-like receptor NKG2D is expressed on cytotoxic CD4+T cells with an effector/memory phenotype, enhancing their TCR-dependent proliferation and cytokine production. A second part of the work is centered on the study of the CD94/NKG2 receptors on NK cells. We show that NKG2A can be induced on NKG2C+ NK cells upon activation with rIL-12 or when cocultured with HCMV-infected dendritic cells, and that NKG2A expression inhibits the response of NKG2C+NK clones against HLA-E-expressing targets, providing a potential regulatory feedback mechanism to control cell activation. Altogether, our results support that expression of NKG2 C-type lectin like receptors may be shaped during the course of viral infections, providing mechanisms to finely regulate both NK and CD4+T cell functions.
Aquesta tesi es centra en l'estudi dels receptors lectina de tipus C NKG2 en cèl·lules Natural Killer i T CD4+. Demostrem que les cèl·lules T CD4+ específiques pel Cytomegalovirus Humà poden expressar diferents receptors NK, i que el receptor lectina tipus C NKG2D s'expressa en cèl·lules citotòxiques i de memòria, potenciant la proliferació i secreció de citocines depenent del TCR. La segona part d'aquesta tesi es centra en l'estudi de l'expressió dels receptors CD94/NKG2 en cèl·lules NK. Mostrem com l'expressió de CD94/NKG2A s'indueix en cèl·lules CD94/NKG2C+ estimulades amb IL-12 o cultivades amb cèl·lules dendrítiques infectades pel Cytomegalovirus Humà, i que l'expressió de CD94/NKG2A inhibeix la resposta de clons NK CD94/NKG2C+ envers dianes HLA-E+, constituint un possible mecanisme de feedback negatiu per controlar l'activació cel·lular. En resum, els nostres resultats demostren que l'expressió dels receptors lectina tipus C NKG2 pot ser modificada durant les infeccions víriques consitutint un possible mecanisme per regular la resposta tant de cèl·lules NK com T CD4+.
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6

Bernhard, Oliver. "Proteomic investigation of the HIV receptors CD4 and DC-SIGN/CD209 membrane protein interactions." Saarbrücken VDM Verlag Dr. Müller, 2004. http://d-nb.info/989278026/04.

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7

Ritsou, Elena. "The role of CD4 and CXCR4 mediated apoptosis in T cell depletion during HIV-1 infection." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390903.

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8

Ghazi, Bouchra. "Réponses cellulaires associées au récepteur KIR3DL2, marqueur spécifique des lymphocytes T tumoraux du syndrome de Sézary." Thesis, Paris Est, 2012. http://www.theses.fr/2012PEST0068.

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Le syndrome de Sézary (SS) est un variant leucémique et érythrodermique de lymphomes T cutanés épidermotropes. Son diagnostic repose à la fois sur des critères cliniques, la présence de lymphocytes T à noyau atypique cérébriforme sur un frottis sanguin et la mise en évidence dans la peau, les ganglions et le sang d’un clone lymphocytaire T CD4+. Notre laboratoire a identifié KIR3DL2 comme premier marqueur membranaire spécifique des cellules tumorales de Sézary. KIR3DL2 peut ainsi être utilisé pour le diagnostic et le suivi des patients atteints du SS. Toutefois, aucune étude n’a démontré de lien entre sa structure de récepteur inhibiteur et sa fonction dans les lymphocytes tumoraux de Sézary, et plus particulièrement son implication possible dans les mécanismes régulant la prolifération et/ou la résistance à l’apoptose des cellules tumorales.Au cours de ce travail deux axes ont été développés :- Un premier axe visant à mieux comprendre la fonction de KIR3DL2 et les mécanismes de signalisation intracellulaire initiés lors de son engagement par l’anticorps AZ158 dans les lymphocytes T tumoraux de Sézary. Nos résultats mettent en évidence un rôle de corécepteur inhibiteur pour KIR3DL2 dans les cellules tumorales de Sézary. En effet, l’engagement de KIR3DL2 inhibe la prolifération et l’AICD induites par la stimulation CD3, cette inhibition étant corrélée à une modulation négative des signaux médiés par le TCR. Ainsi, KIR3DL2 ne se comporte pas comme une unité de signalisation indépendante dans les cellules tumorales de Sézary, contrairement à ce qui est observé dans les cellules NK.- Un second axe portant sur l’évaluation d’une nouvelle fonction de KIR3DL2 comme récepteur pour les ODN CpG. Ainsi, nous rapportons pour la première fois un effet direct de l’ODN CpG sur les cellules tumorales T CD4+ de Sézary. En effet, nous avons observé un effet apoptotique de l’ODN CpG-C caspases-dépendant sur les lignées et les cellules tumorales circulantes. De plus, le traitement des cellules tumorales de patients Sézary avec l’ODN CpG-C conduit à une inhibition de l’activation constitutive du facteur de transcription STAT3.La réalisation de cette étude a permis de mieux comprendre la fonction et les mécanismes initiés à partir de KIR3DL2 dans les cellules tumorales T CD4+ de Sézary. De plus, ce travail ouvre de nouvelles perspectives thérapeutiques basées sur le ciblage direct et spécifique des cellules tumorales de Sézary pouvant être associé à une stimulation des acteurs immuns grâce à l’action des ODN CpG
Sézary syndrome (SS) is an aggressive leukemic and erythrodermic variant of cutaneous T-cell lymphoma. It is characterized by the presence of a clonal CD4+ T lymphocyte population in the skin, lymph nodes and peripheral blood. Our laboratory has previously identified the NK cell receptor KIR3DL2 as a valuable diagnostic and prognostic marker for the detection of the tumoral T cell burden of Sézary syndrome patients. However, the function of this receptor on the malignant T lymphocyte population remained unexplored. The specific expression of KIR3DL2 by SS patients malignant cells prompted us to investigate its possible influence on mechanisms regulating the tumoral cells outgrowth and apoptosis process.To this aim, two axes were developed. The first axis aimed to highlight the function of KIR3DL2 on the malignant T lymphocyte population and to elucidate the intracellular signaling mechanisms initiated by engagement of the receptor with the monoclonal antibody AZ158. Our results show that KIR3DL2 can exert an inhibitory co-receptor function in malignant Sézary cells. Indeed, triggering of KIR3DL2 inhibits the CD3-mediated proliferation and cell death of the CD4+ KIR3DL2+ cells, this inhibition being correlated to a down-modulation of the TCR-mediated signals. Thus, KIR3DL2 does not behave as an independent signaling unit in Sézary cells, unlike NK cells.The second axis aimed to evaluate a new function of KIR3DL2 as CpG ODN receptor. We show for the first time a direct effect of CpG ODN on tumoral CD4+ T Sézary cells. Thus, we observed a caspase-dependent apoptotic effect of CpG ODN-C on Sézary cell lines and circulating malignant T cells. This process of cellular death is correlated to a dephosphorylation of the transcription factor STAT3, which is found constitutively phosphorylated and activated in Sézary cells.This study has provided new insights into the function and the intracellular signaling pathways initiated by KIR3DL2 in malignant Sézary T cells. Furthermore, this work opens new therapeutic perspectives based on the direct and specific targeting of tumor cells that could be associated to immune cell stimulation through the use of ODN CpG
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Fickinger, Andira Michele da Cruz. "Papel dos receptores de glutamato tipo NMDA em macrófagos, células dendríticas e células T CD4 ativadas in vitro." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-11072014-091556/.

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A neuroimunologia é o ramo da imunologia que estuda a relação entre sistema imune e o sistema nervoso. Muitos estudos têm demonstrado a capacidade direta de neurotransmissores em modular a resposta imune, assim como de citocinas em influenciar funções cognitivas. Neste contexto, o glutamato possui papel de destaque, por se tratar do neurotransmissor excitatório mais importante e mais abundante no sistema nervoso central dos mamíferos. Sua função é exercida através de dois tipos de receptores principais: i) os receptores ionotrópicos (iGluR) e ii) os receptores metabotrópicos (mGluR). A descoberta da expressão de receptores de glutamato em células do sistema imune tem despertado interesse científico, levantando questões acerca de sua expressão e função. No presente trabalho, avaliamos parâmetros como viabilidade celular, linfoproliferação e ativação de MAP quinase pelo receptor NMDAR esplenócitos totais e linfócitos cultivados in vitro. Nossos resultados demonstram que linfócitos em repouso e ativados apresentam diferentes perfis de expressão do receptor NMDAR. O uso do antagonista deste receptor, o MK801, foi capaz de reduzir a proliferação de linfócitos T CD4 e T CD8 estimulados com anti-CD3 em cultura de esplenócitos. Tal redução pode ser explicada por um aumento na taxa de morte celular, o que foi avaliado através de marcação com anexina-V, indicador de apoptose, ou 7-AAD, indicador de necrose. Para entendermos um pouco a respeito da sinalização do receptor NMDAR no sistema imune, avaliamos a fosforilação da MAP quinase ERK 1,2 em linfócitos T CD4 ativados na presença do agonista (NMDA) ou do antagonista (MK801) do receptor. Observamos um aumento na ativação desta quinase na presença de NMDA, o que é revertido na presença do MK801. Ao avaliar o papel do receptor NMDAR in vivo, verificamos uma redução significativa na gravidade da encefalomielite experimental auto-imune em animais tratados com MK801. Mais interessante, esta redução se correlaciona também com uma redução na fosforilação de ERK 1,2 em esplenócitos totais obtidos ao dia 7 pós-imunização. Em resumo, nossos dados sugerem que o receptor NMDA possui o papel de ativador de vias intracelulares importantes, como as da MAP quinase ERK 1,2; e que o seu bloqueio resulta em morte celular in vitro. Logo, isso indica a importância do glutamato como modulador da intensidade da resposta e viabilidade de linfócitos T CD4 e T CD8 in vitro e in vivo. Sendo assim, nossos resultados contribuem para um melhor entendimento dos fenômenos de imunoregulação, especialmente aqueles no campo da neuroimunologia ou neuroimunomodulação.
Neuroimmunology is a field within immunology which studies the relationship between the nervous system and the immune system. Several studies have demonstrated the direct ability of neurotransmitters in modulating the immune response, as for cytokines in influencing cognitive functions. In this context, glutamate stands out for being the most important and abundant neurotransmitter in the mammal central nervous system. Its role is exerted through two main types of receptor: i) ionotropic receptors (iGluR) and ii) metabotropic receptors (mGluR). The discovery of glutamate receptor expression in immune cells has led to scientific interest, raising issues concerning its expression and function. In the present study, we evaluated parameters such as cell viability, lymphoproliferation, and activation of the MAP quinase pathway by the NMDA receptor on total splenocytes and lymphocytes cultured in vitro. Our results demonstrate that naive and activated lymphocytes present different profiles of NMDA receptor expression. The use of MK801, an antagonist for this receptor, was able to reduce the T CD4 and T CD8 lymphocyte proliferation stimulated with anti-CD3 in splenocyte culture. Such reduction may be explained by the increase of the cellular death rate, evaluated by annexin-V staining, indicator of apoptosis or 7-AAD, indicator of necrosis. With the intent of understanding part of the NMDA receptor signaling in the immune system, we evaluated the ERK 1,2 MAP quinase phosphorylation in T CD4 lymphocytes activated in the presence of the agonist (NMDA) or the antagonist (MK801) of the receptor. We observed an increase in this quinase activation in the presence of NMDA, which is reversed by the MK801. When evaluating the role of the NMDA receptor in vivo, we verified a significant reduction in the degree of experimental auto-immune encephalomyelitis in animals treated with MK801. More interesting, this reduction also correlates to a reduction on the phosphorilation of ERK 1,2 in total splenocytes obtained at the seventh day post-immunization. In sum, our data suggest that the NMDA receptor has the role of activating important intracellular pathways, such as the MAP quinases ERK 1,2; and that its blockage results in cellular death in vitro. As so, this indicates the importance of glutamate as a modulator of the intensity of response and the viability of T CD4 e T CD8 lymphocytes in vitro e in vivo. Thus, our result contribute for a better understanding of the immunoregulation phenomena, especially those in the neuroimmunology ou neuroimmunomodulation field.
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Deftos, Michael Laing. "Notch signaling in T cell development /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/8364.

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Books on the topic "CD4 Receptors"

1

Teale, Glyn Robert. Characterisation of the CD40 cell surface receptor in cervical invasive and preinvasive disease. Birmingham: University of Birmingham, 2001.

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Adhesion-GPCRs structure to function. New York, N.Y: Springer Science+Business Media, 2010.

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Kyewski, B., and Elisabeth Suri-Payer. CD4+CD25+ Regulatory T Cells: Origin, Function and Therapeutic Potential. Springer, 2010.

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(Editor), B. Kyewski, and Elisabeth Suri-Payer (Editor), eds. CD4+CD25+ Regulatory T Cells: Origin, Function and Therapeutic Potential (Current Topics in Microbiology and Immunology). Springer, 2005.

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Livingston, Schuyler, Benjamin Young, Martin Markowitz, Poonam Mathur, and Bruce L. Gilliam. HIV Virology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0017.

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HIV is a member of the lentivirus subfamily of retroviruses. Two distinct groups of viruses are pathogenic in humans: HIV-1 and HIV-2. Both are transmitted sexually and known to cause immunodeficiency disease. HIV enters the cell through use of the CD4 receptor and chemokine co-receptors, primarily CCR5 and CXCR4. The viral genome is transcribed from RNA to DNA by reverse transcriptase and integrated into the host genome by integrase. The HIV genome encodes 15 proteins, comprising three categories: structural, regulatory, and accessory. After budding from the host cell, the virus matures into its infectious form through cleavage of viral precursor proteins by protease.
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Goldstein, Marni Diane. Differential signal transduction by the B cell activation receptor CD40. 1998.

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Naor, David, ed. Interaction between Hyaluronic Acid and Its Receptors (CD44, RHAMM) Regulates the Activity of Inflammation and Cancer. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-913-6.

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Branch, Moody D., ed. T cell activation by CD1 and lipid antigens. Berlin: Springer, 2007.

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Veskler, Barbara A. New Research On Immunology. Nova Biomedical Books, 2005.

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1953-, Gordon J., ed. CD23--a novel multifunctional regulator of the immune system that binds IgE. Basel: Karger, 1991.

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Book chapters on the topic "CD4 Receptors"

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Aszalos, A., P. S. Pine, and J. Weaver. "Polyionic Compounds Selectively Alter Availability of CD4 Receptors for HIV Coat Protein rgp 120." In Molecular Aspects of Chemotherapy, 209–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-662-02740-0_14.

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Su, S. B., H. Ueda, O. M. Z. Howard, M. C. Grimm, W. Gong, F. W. Ruscetti, J. J. Oppenheim, and J. M. Wang. "Inhibition of the Expression and Function of Chemokine Receptors on Human CD4+ Leukocytes by HIV-1 Envelope Protein gp120." In Chemical Immunology and Allergy, 141–60. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000058731.

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Riedel, D., M. Brach, R. Mertelsmann, and F. Herrmann. "Surface Expression of Interleukin-2 Receptors and CD4 Molecules by Human Eosinophils is Induced by GM-CSF and IL-3." In Cytokines in Hemopoiesis, Oncology, and AIDS, 59–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75510-1_8.

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Hait, Nitai C., Sheldon Milstien, and Sarah Spiegel. "Identification of Direct Intracellular Targets of Sphingosine 1-Phosphate (S1P)." In Lysophospholipid Receptors, 71–83. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118531426.ch4.

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Ashorn, Per, Bernard Moss, and Edward A. Berger. "Therapeutic Strategies Employing CD4, the HIV Receptor." In Advances in Experimental Medicine and Biology, 71–81. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3462-4_6.

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Luckey, Megan A., and Jung Hyun Park. "Cytokine Receptor Signaling and CD4/CD8 Lineage Choice during T Cell Development in the Thymus." In Mathematical, Computational and Experimental T Cell Immunology, 1–20. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57204-4_1.

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Söderström, Kalle. "HSP60-peptide interference with CD94/NKG2 receptors." In Heat Shock Proteins and Inflammation, 257–72. Basel: Birkhäuser Basel, 2003. http://dx.doi.org/10.1007/978-3-0348-8028-2_17.

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Ikeda, Hiroshi. "Fluorescent Cyclodextrins as Chemosensors for Molecule Detection in Water." In Artificial Receptors for Chemical Sensors, 113–34. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2010. http://dx.doi.org/10.1002/9783527632480.ch4.

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Greenberg, Steven, and Benjamin M. Dale. "Fc Receptors and Phagocytosis." In Phagocyte-Pathogen Interactions, 69–92. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816650.ch4.

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Singh, Mark D., Robert J. B. Nibbs, and Gerard J. Graham. "The Atypical Chemokine Receptors." In Methods and Principles in Medicinal Chemistry, 67–83. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527631995.ch4.

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Conference papers on the topic "CD4 Receptors"

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Kisielow, Jan, Franz-Josef Obermair, and Manfred Kopf. "Abstract B078: Unbiased identification of CD4+ T-cell epitopes using novel MHC-based chimeric receptors." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-b078.

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Slavoljub, Milosevic, Ellinger Christian, Wehner Carina, Raffegerst Silke, Wilde Susanne, Weis Manon, Sailer Nadja, and Schendel Dolores. "Abstract A017: Method for molecular characterization of antigens, epitopes and T cell receptors for adoptive CD4 immunotherapy." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a017.

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Sennino, Barbara, Andrew Conroy, Bhamini Purandare, Kyle Jacoby, Olivier Dalmas, Songming Peng, Alex Franzusoff, and Stefanie Mandl. "Abstract 895: Coexpression of MHC class I-restricted neoTCRs and ectopic CD8 receptors in precision genome engineered CD4 T cells significantly potentiates antigen-specific effector functions." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-895.

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Smith, Duane, Payal Watchmaker, Guido Stadler, Natalie Marks, Yelena Bronevetsky, Keviin Chapman, and Hideho Okada. "Abstract 5773: Sequencing and cloning IDH1 R132H-targeted monoclonal T cell receptors from CD4+T cells facilitated by opto-electric-positioning technology." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5773.

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Barbosa, Karen Eduarda. "DESDOBRAMENTOS DA RESPOSTA IMUNOLÓGICA FRENTE À INFECÇÃO PELO VÍRUS DO HIV: UMA REVISÃO SISTEMÁTICA." In I Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/948.

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INTRODUÇÃO: Segundo os dados do boletim epidemiológico do Ministério da Saúde, foram notificados 342.459 casos de infecção pelo vírus HIV no Brasil, entre os períodos de junho de 2007 a junho de 2020, demonstrando uma grande incidência da doença no país. Cabe salientar que o vírus é capaz de degradar as células do sistema imunológico, levando ao processo de imunossupressão, deixando o organismo suscetível a doenças oportunistas. OBJETIVOS: O estudo irá avaliar os mecanismos da resposta imune frente a uma invasão pelo vírus do HIV, por meio de um levantamento bibliográfico. METODOLOGIA: O presente trabalho tratou-se de um estudo descritivo que fez uso da base de dados do portal PUBMED, por meio da combinação das seguintes palavras chaves: HIV infection, CD4+ T cells, immune response e review. No total, foram disponibilizados 16 artigos pela plataforma para recuperação dos dados. RESULTADOS: Os mecanismos de defesa contra a infecção pelo HIV iniciam com a entrada do vírus pela barreira epitelial, mediados por receptores de quimiocinas CCR5 e CXCR4 e a molécula de superfície celular CD4. Ocorre o encontro com as células dendríticas, por meio do reconhecimento PAMP-TLR e a maturação das mesmas, que irão conduzir os antígenos aos linfonodos, iniciando a apresentação aos linfócitos T que, num contexto favorável, se ativam. Por meio do processo de sinapse infecciosa, os vírus podem comprometer os linfócitos T-CD4+ de memória efetora – seu principal alvo. A perda desses linfócitos ocorre por apoptose dependente caspase-3 após a produção de novos vírions. É esse processo de morte celular que impulsiona a progressão clínica para a síndrome da imunodeficiência adquirida (AIDS). Nas primeiras semanas após a infecção, ressalta-se que a viremia aguda também é responsável pela ativação de células T-CD8+. Ressalta-se também que o sistema imune inato contribui nesse processo, uma vez que reconhecerá o RNA viral ativando respostas, como a expressão do IFN- tipo I e interleucinas. No entanto, o vírus se aproveita dessa situação, criando um ambiente favorável para sua replicação. CONCLUSÕES: As infecções oportunistas que ocorrem em pacientes HIV/AIDS estão relacionadas sobretudo à depleção de linfócitos T CD4+ que o vírus provoca.
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Ohnishi, Hiroshi, Nobuaki Miyahara, Katsuyuki Takeda, Anthony Joetham, Akihito Yokoyama, and Erwin W. Gelfand. "Synergistic Effects Of CD4+ And CD8+ T Cells For The Full Development Of Allergen-Induced Airway Hyperresponsiveness Requires Leukotriene B4 Receptor-1 Expression." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2571.

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Ahmed, Sumaya, and Nasser Rizk. "The Expression of Bile Acid Receptor TGR5 in Adipose Tissue in Diet-Induced Obese Mice." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0212.

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Bile acids are significant physiological factors for digestion, solubilization, absorption, toxic metabolites and xenobiotics. In addition, bile acids are responsible of signal transduction as well as metabolic regulation that activate several receptors such as farnesoid X receptor (FXR) and the membrane G-protein receptor 5 (TGR5). Activation of TGR5 by bile acids is associated with prevention of obesity as well as ameliorating the resistance to insulin via increasing energy expenditure. The objective of this research is to investigate TGR5 gene expression level in different fat depots including visceral or epididymal adipose tissue (eWAT), brown adipose tissue and inguinal adipose tissue (iWAT) and to study the response of TGR5 gene expression to the antiobesity treatment (SFN). Three groups of male CD1 mice were used in this study; lean group fed with SCD, DIO mice on HFD and DIO obese mice treated with anti-obesity treatment. Body weight (BW) and phenotype data were evaluated by weekly including blood samples for analysis of glucose, insulin, leptin, triglycerides (TG). Total RNA was extracted from different fat depots and RT-PCR profiler array technology was used to in order to assess the mRNA expression of TGR5 and leptin. There was significant downregulation of TGR5 gene expression level in obese (DIO) mice and remarkable upregulation of TGR5 gene expression after successful weight loss in DIO mice treated with SFN in time dependent manner at 1 weeks and 4 weeks of ip applications. In conclusion, obesity is associated with decrease in expression of TGR5 in different fat depots and treatment with anti-obesity drug (Sulforaphane) causes stepwise upregulation of TGR5 gene expression in epididymal white adipose tissue parallel stepwise decrease in body weight. Increase of expression of TGR5 in DIO mice in eWAT is accompanied by improvement in glucose homeostasis and insulin action.
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Koya, Richard C., Thinle Chodon, Junko Matsuzaki, Takemasa Tsuji, Satoko Matsueda, and Kunle Odunsi. "Abstract LB-186: Sustained efficacy of immunotherapy for solid tumors with novel dual CD4/CD8 T cell receptor engineered synergistic combination of hematopoietic stem cells and T cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-186.

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da Silva, Larissa Amoroso, Rogério Rodrigo Ramos, and Luciana Estevam Simonato. "FILOGENIA E MECANISMOS DA PATOGÊNESE DE SARS-COV-2: ESTUDO SISTEMÁTICO." In I Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/632.

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Introdução: O SARS-CoV-2 é um membro da família dos coronavírus; eles são vírus de RNA de fita única, geneticamente diversos, que evoluem e sofrem mutações rapidamente, comumente infectando humanos. Objetivos: Devido ao surto atual de coronavírus, o presente estudo teve como objetivo realizar uma ampla revisão da evolução do vírus, bem como dos mecanismos que levaram ao desenvolvimento do SARS-CoV-2. Material e métodos: Para esta pesquisa, 469 estudos foram inicialmente selecionados e submetidos à análise de elegibilidade; desses estudos, 164 foram selecionados para uma avaliação mais criteriosa e, ao final desse processo, foram escolhidos 52 estudos para serem discutidos, seguindo as diretrizes do PRISMA para revisões sistemáticas. Resultados: Estudos recentes demonstraram que o genoma SARS-CoV-2 e o vírus RaTG13 são mais de 90% semelhantes entre si, que indica que o genoma do morcego (Bat-SL-CoVZC45 e Bat-SL-CoVZXC21) e o genoma dos pangolins (pangolin-CoV GD / P1L e pangolin-CoV GD / P2S) compartilham a mesma ancestralidade do genoma humano, portanto, esses animais são considerados responsáveis por espalhar o novo vírus para humanos; isso pode eliminar a teoria de que o SARS-CoV-2 foi um vírus feito em laboratório. Conclusão: A infecção começa quando o vírus se liga ao receptor de células ACE2 e se prolifera para células epiteliais da mucosa nasal e pneumócitos do tipo II, resultando em um aumento da quantidade de citocinas (IL-6, IL-10 e TNF-α) e uma diminuição da quantidade de linfócitos (células T CD4+ e CD8+).
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Al Heialy, S., B. Tolloczko, K. Tsuchiya, S. Siddiqui, D. Ramos-Barbon, and JG Martin. "Antigen-Specific CD4+ T Cells Drive Airway Smooth Muscle Proliferation through the Epidermal Growth Factor Receptor." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5598.

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Reports on the topic "CD4 Receptors"

1

Weinberg, Andrew D. Tumor Specific CD4+ T-Cell Costimulation Through a Novel Receptor/Ligand Interaction. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada374764.

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Weinberg, Andrew D. Tumor Specific CD4+ T-Cell Costimulation Through a Novel Receptor Ligand Interaction. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada359629.

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Weber, George F. Contribution of the Receptor/Ligand Interaction Between CD44 and Osteopontin to Formation of Breast Cancer Metastases. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada384133.

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Weber, Georg. Contribution of the Receptor/Ligand Interaction Between CD44 and Osteopontin to Formation of Breast Cancer Metastases. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada393323.

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