Relevant bibliographies by topics / CD30+/CD30L T cell

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Academic literature on the topic 'CD30+/CD30L T cell'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "CD30+/CD30L T cell"

1

Younes, A., U. Consoli, V. Snell, et al. "CD30 ligand in lymphoma patients with CD30+ tumors." Journal of Clinical Oncology 15, no. 11 (1997): 3355–62. http://dx.doi.org/10.1200/jco.1997.15.11.3355.

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PURPOSE CD30 ligand (CD30L), which is expressed on resting B and activated T lymphocytes, can induce cell death in several CD30+ cell lines. Patients with CD30+ tumors (Hodgkin's disease and Ki-1+ non-Hodgkin's lymphoma) frequently have elevated soluble CD30 (sCD30) levels in their serum, which correlates with a poor prognosis. The role of sCD30 in protecting tumor cells from CD30L-mediated cell death and the pattern of CD30L expression on human peripheral-blood lymphocytes (PBLs) of normal donors and patients with CD30+ tumors are investigated. MATERIALS AND METHODS CD30L surface protein expression was determined by two-color flow cytometry on PBLs of patients with CD30+ tumors and normal individuals. CD30L levels were determined on subsets of PBLs before and after stimulation with phytohemagglutinin (PHA), anti-CD3 antibody, or CD40L. sCD30 was measured by enzyme-linked immunosorbent assay (ELISA). The apoptotic activity of membrane-bound CD30L was tested in a CD30+ cell line by the annexin V-binding method. RESULTS Unstimulated T lymphocytes of normal donors and patients with lymphoma rarely expressed CD30L surface protein, but were able to express it after stimulation with PHA or anti-CD3 antibody. Resting B cells of patients with CD30+ tumors had lower levels of detectable surface CD30L compared with normal donors (mean, 55% and 80.6%, respectively; P = .0008). Patients with high levels of serum sCD30 had lower detectable levels of CD30L on their PBLs (R2 = .72, P = .0008) and exogenous sCD30 blocked membrane-bound CD30L-mediated apoptosis in a CD30+ cell line. CONCLUSION In patients with CD30+ tumors, sCD30 can decrease the availability of CD30L on PBLs. Blocking the apoptosis-inducing activity of CD30L by its soluble receptor may explain how CD30+ tumors escape immunosurveillance and may be related to the reported poor prognosis of patients who have elevated sCD30 levels.
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Willis, Cynthia R., Yi-Ling Hu, Anh Leith, and James B. Rottman. "CD30 / CD30L interactions promote class-switched antibody responses to T-dependent antigens (34.3)." Journal of Immunology 182, no. 1_Supplement (2009): 34.3. http://dx.doi.org/10.4049/jimmunol.182.supp.34.3.

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Abstract The cell-surface glycoproteins CD30 and CD30L are members of the TNFR and TNF superfamilies, respectively. CD30 is expressed on subpopulations of activated T and B cells. CD30L is expressed on activated T cells, macrophages, and dendritic cells, as well as germinal center B cells. CD30 / CD30L interactions provide activation-induced costimulatory signals that sustain T-cell responses, mediate B-cell activity, and generate long-lived memory T cells for chronic B-cell help. Although other activation-induced costimulatory molecules induce antibody isotype class switching, it is less clear what the function is of CD30 signaling on class switching and antibody production. Therefore, we tested the effect of in vivo blockade of the CD30 / CD30L pathway on antibody class switching in response to T-dependent antigens using two systems that require activated-T cells to stimulate B-cell responses. First, BALB/c mice immunized with a T-dependent antigen and treated with anti-CD30L antibodies produced less antigen-specific antibodies of IgG1 and IgE isotypes as compared to control-treated mice, whereas antigen-specific antibodies of the IgM isotype were similar in all groups. Likewise, NZB/W F1 lupus-prone mice treated with anti-CD30L antibodies produced less anti-dsDNA antibodies of the IgG1 and IgG2a isotypes as compared to control-treated mice, whereas anti-dsDNA antibodies of the IgM isotype were similar in all groups. In both systems, specific subpopulations of lymphocytes necessary for responses to T-dependent antigens were reduced by blockade of the CD30 / CD30L pathway. Our results demonstrate that CD30 / CD30L interactions positively regulate T-cell dependent B-cell responses necessary for class-switched antibody responses.
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Mori, M., C. Manuelli, N. Pimpinelli, et al. "CD30-CD30 Ligand Interaction in Primary Cutaneous CD30+T-Cell Lymphomas: A Clue to the Pathophysiology of Clinical Regression." Blood 94, no. 9 (1999): 3077–83. http://dx.doi.org/10.1182/blood.v94.9.3077.

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Abstract Primary CD30+ cutaneous T-cell lymphomas (CTCLs) represent a spectrum of non-Hodgkin’s lymphomas (NHLs) that have been well defined at the clinical, histologic, and immunologic level. This group, which includes 2 main entities (large cell lymphoma and lymphomatoid papulosis [LyP]) and borderline cases, is characterized by the expression of CD30 antigen by neoplastic large cells at presentation, possible spontaneous regression of the skin lesions, and generally favorable clinical course. Although the functional relevance of CD30 and its natural ligand (CD30L) expression in most cases of NHL is presently undefined, previous studies indicate that CD30L is likely to mediate reduction of proliferation in CD30+ anaplastic large-cell NHL. No information is currently available concerning the expression of CD30L in primary CD30+ CTCLs. In this study, we investigated the immunophenotypic and genotypic expression of CD30 and CD30L in different developmental phases of skin lesions (growing v spontaneously regressing). By immunohistochemistry, CD30L expression was detected in regressing lesions only; by molecular analysis, the expression of CD30L was clearly higher in regressing lesions than in growing ones. CD30L, while expressed by some small lymphocytes, was most often coexpressed by CD30+neoplastic large cells, as demonstrated by 2-color immunofluorescence and by immunohistochemistry on paraffin sections. Taken together, these data suggest that CD30-CD30L interaction may play a role in the pathobiology of primary cutaneous CD30+lymphoproliferative disorders. In particular, CD30L (over)expression might have a major role in the mechanism of self-regression of skin lesions, the most distinctive clinical feature of this cutaneous lymphoma subtype.
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Mori, M., C. Manuelli, N. Pimpinelli, et al. "CD30-CD30 Ligand Interaction in Primary Cutaneous CD30+T-Cell Lymphomas: A Clue to the Pathophysiology of Clinical Regression." Blood 94, no. 9 (1999): 3077–83. http://dx.doi.org/10.1182/blood.v94.9.3077.421k28_3077_3083.

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Primary CD30+ cutaneous T-cell lymphomas (CTCLs) represent a spectrum of non-Hodgkin’s lymphomas (NHLs) that have been well defined at the clinical, histologic, and immunologic level. This group, which includes 2 main entities (large cell lymphoma and lymphomatoid papulosis [LyP]) and borderline cases, is characterized by the expression of CD30 antigen by neoplastic large cells at presentation, possible spontaneous regression of the skin lesions, and generally favorable clinical course. Although the functional relevance of CD30 and its natural ligand (CD30L) expression in most cases of NHL is presently undefined, previous studies indicate that CD30L is likely to mediate reduction of proliferation in CD30+ anaplastic large-cell NHL. No information is currently available concerning the expression of CD30L in primary CD30+ CTCLs. In this study, we investigated the immunophenotypic and genotypic expression of CD30 and CD30L in different developmental phases of skin lesions (growing v spontaneously regressing). By immunohistochemistry, CD30L expression was detected in regressing lesions only; by molecular analysis, the expression of CD30L was clearly higher in regressing lesions than in growing ones. CD30L, while expressed by some small lymphocytes, was most often coexpressed by CD30+neoplastic large cells, as demonstrated by 2-color immunofluorescence and by immunohistochemistry on paraffin sections. Taken together, these data suggest that CD30-CD30L interaction may play a role in the pathobiology of primary cutaneous CD30+lymphoproliferative disorders. In particular, CD30L (over)expression might have a major role in the mechanism of self-regression of skin lesions, the most distinctive clinical feature of this cutaneous lymphoma subtype.
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Barbieri, Alessandro, Marzia Dolcino, Elisa Tinazzi, et al. "Characterization of CD30/CD30L+Cells in Peripheral Blood and Synovial Fluid of Patients with Rheumatoid Arthritis." Journal of Immunology Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/729654.

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The CD30/CD30L signalling system has been implicated in the pathogenesis of several autoimmune and inflammatory conditions. In rheumatoid arthritis (RA), soluble CD30 (sCD30) levels reflect the recruitment of CD30+T cells into the inflamed joints and correlate with a positive response to immunosuppressive therapy. The aim of our report was to clarify the role of CD30/CD30L signalling system in the pathogenesis of RA. Our analysis of the CD30L+T cell subsets in peripheral blood (PB) and synovial fluid (SF) of RA patients and of the related cytokine profiles suggests the involvement of CD30/CD30L signalling in polarization of T cells towards a Th17 phenotype with proinflammatory features. Moreover, in RA SF nearly 50% of Treg cells express CD30, probably as an attempt to downmodulate the ongoing inflammation. We also show here that the engagement of CD30L on neutrophils stimulated with CD30/Fc chimera may play a crucial role in RA inflammation since activated neutrophils release IL-8, thus potentially amplifying the local inflammatory damage. In conclusion, the results obtained suggest that the complex CD30/CD30L signalling pathway is implicated in the pathogenesis and progression of RA synovitis through a concerted action on several immune effector cells.
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Romagnani, Paola, Francesco Annunziato, Roberto Manetti, et al. "High CD30 Ligand Expression by Epithelial Cells and Hassal's Corpuscles in the Medulla of Human Thymus." Blood 91, no. 9 (1998): 3323–32. http://dx.doi.org/10.1182/blood.v91.9.3323.

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Abstract CD30 is a member of tumor necrosis factor (TNF) receptor superfamily that is expressed by activated T cells in the presence of interleukin-4 (IL-4). Although CD30 can mediate a variety of signals, CD30-deficient mice have impaired negative selection of T cells, suggesting that at least in the context of murine thymus, CD30 is a cell death–mediating molecule. The ligand for CD30 (CD30L) is a membrane-associated glycoprotein related to TNF, which is known to be expressed mainly by activated T cells and other leukocytes. However, the nature of CD30L-expressing cells involved in the interaction with CD30+ thymocytes is unclear. We report here that in postnatal human thymus the great majority of CD30+ cells are double positive (CD4+CD8+), activated, IL-4 receptor–expressing T cells which selectively localize in the medullary areas. Moreover, many medullary epithelial cells and Hassal's corpuscles in the same thymus specimens showed unusually high expression of CD30L in comparison with other lymphoid or nonlymphoid tissues. These findings provide additional information on the nature and localization of CD30+ thymocytes and show that epithelial cells are the major holder of CD30L in the thymic medulla.
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Romagnani, Paola, Francesco Annunziato, Roberto Manetti, et al. "High CD30 Ligand Expression by Epithelial Cells and Hassal's Corpuscles in the Medulla of Human Thymus." Blood 91, no. 9 (1998): 3323–32. http://dx.doi.org/10.1182/blood.v91.9.3323.3323_3323_3332.

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CD30 is a member of tumor necrosis factor (TNF) receptor superfamily that is expressed by activated T cells in the presence of interleukin-4 (IL-4). Although CD30 can mediate a variety of signals, CD30-deficient mice have impaired negative selection of T cells, suggesting that at least in the context of murine thymus, CD30 is a cell death–mediating molecule. The ligand for CD30 (CD30L) is a membrane-associated glycoprotein related to TNF, which is known to be expressed mainly by activated T cells and other leukocytes. However, the nature of CD30L-expressing cells involved in the interaction with CD30+ thymocytes is unclear. We report here that in postnatal human thymus the great majority of CD30+ cells are double positive (CD4+CD8+), activated, IL-4 receptor–expressing T cells which selectively localize in the medullary areas. Moreover, many medullary epithelial cells and Hassal's corpuscles in the same thymus specimens showed unusually high expression of CD30L in comparison with other lymphoid or nonlymphoid tissues. These findings provide additional information on the nature and localization of CD30+ thymocytes and show that epithelial cells are the major holder of CD30L in the thymic medulla.
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Rottman, James B., Yi-Ling Hu, and Cynthia Willis. "Blockade of the CD30/CD30L pathway inhibits renal disease in young, SLE-prone NZB/W F1 mice (50.41)." Journal of Immunology 182, no. 1_Supplement (2009): 50.41. http://dx.doi.org/10.4049/jimmunol.182.supp.50.41.

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Abstract CD30 and CD30L are interacting members of the TNFR and TNF family, respectively. CD30 is expressed by subsets of activated T and B cells, whereas CD30L is expressed by subsets of activated T cells, macrophages and dendritic cells. The CD30 / CD30L interaction modulates T cell activation, germinal center formation and antibody isotype class switching. Given the importance of this pathway to B cell function, we tested the hypothesis that blockade of the CD30 / CD30L pathway would decrease or abrogate autoantibody formation and renal disease in the NZB/W F1 murine model of systemic lupus erythematosis (SLE). Young (5 mo) NZB/W F1 mice were treated with 300 μg CD30L blocking (M15-N297A) or blocking / depleting (M15-IgG2a) antibody weekly for 3 months during the onset of autoimmunity. Both treatments a) reduced the onset and severity of proteinuria, b) significantly decreased the severity of renal histologic scores, c) decreased glomerular immune complex and complement deposition and d) these effects were associated with reduced production of anti-DNA antibodies of the IgG, but not IgM isotype. CD30 / CD30L blockade may be a viable approach for the treatment of SLE.
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9

Gattei, Valter, Massimo Degan, Annunziata Gloghini, et al. "CD30 Ligand Is Frequently Expressed in Human Hematopoietic Malignancies of Myeloid and Lymphoid Origin." Blood 89, no. 6 (1997): 2048–59. http://dx.doi.org/10.1182/blood.v89.6.2048.

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Abstract CD30 ligand (CD30L) is a type-II membrane glycoprotein capable of transducing signals leading to either cell death or proliferation through its specific counterstructure CD30. Although several lines of evidence indicate that CD30L plays a key role as a paracrine- or autocrine-acting surface molecule in the deregulated cytokine cascade of Hodgkin's disease, little is known regarding its distribution and biologic significance in other human hematopoietic malignancies. By analyzing tumor cells from 181 patients with RNA studies and immunostaining by the anti-CD30L monoclonal antibody M80, we were able to show that human hematopoietic malignancies of different lineage and maturation stage display a frequent and broad expression of the ligand. CD30L mRNA and surface protein were detected in 60% of acute myeloid leukemias (AMLs), 54% of B-lineage acute lymphoblastic leukemias (ALLs), and in a consistent fraction (68%) of B-cell lymphoproliferative disorders. In this latter group, hairy cell leukemia and high-grade B-cell non-Hodgkin's lymphoma (B-NHL) expressed a higher surface density of CD30L as compared with B-cell chronic lymphocytic leukemia and low-grade B-NHL. Purified plasmacells from a fraction of multiple myeloma patients also displayed CD30L mRNA and protein. A more restricted expression of CD30L was found in T-cell tumors that was mainly confined to neoplasms with an activated peripheral T-cell phenotype, such as T-cell prolymphocytic leukemia, peripheral T-NHL, and adult T-cell leukemia/lymphoma. In contrast, none of the T-lineage ALLs analyzed expressed the ligand. In AML, a high cellular density of CD30L was detected in French-American-British M3, M4, and M5 phenotypes, which are directly associated with the presence on tumor cells of certain surface structures, including the p55 interleukin-2 receptor α-chain, the αM (CD11b) chain of β2 integrins, and the intercellular adhesion molecule-1 (CD54). Analysis of normal hematopoietic cells evidenced that, in addition to circulating and tonsil B cells, a fraction of bone marrow myeloid precursors, erythroblasts, and subsets of megakaryocytes also express CD30L. Finally, we have shown that native CD30L expressed on primary leukemic cells is functionally active by triggering both mitogenic and antiproliferative signals on CD30+ target cells. As opposed to CD30L, only 10 of 181 primary tumors expressed CD30 mRNA or protein, rendering therefore unlikely a CD30-CD30L autocrine loop in human hematopoietic neoplasms. Taken together, our data indicate that CD30L is widely expressed from early to late stages of human hematopoiesis and suggest a regulatory role for this molecule in the interactions of normal and malignant hematopoietic cells with CD30+ immune effectors and/or microenvironmental accessory cells.
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Wiley, S. R., R. G. Goodwin, and C. A. Smith. "Reverse signaling via CD30 ligand." Journal of Immunology 157, no. 8 (1996): 3635–39. http://dx.doi.org/10.4049/jimmunol.157.8.3635.

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Abstract CD30 ligand (CD30L), a member of the TNF family, is a type II membrane protein with a C-terminal extracellular domain that is homologous with the extracellular domains of other TNF family members. Also, like most TNF family members, the N-terminal cytoplasmic domain of CD30L is conserved across species, but not between family members, suggesting a possible biological function. Motivated by this observation, we investigated the potential for CD30L, when activated by cross-linking, to directly transduce a signal to the ligand-bearing cell. Cross-linking of CD30L by a mAb or by CD30-Fc fusion protein induced the production of IL-8 by freshly isolated neutrophils. Further, both cross-linking mechanisms produced a rapid oxidative burst. Indirect effects through CD30 were ruled out, since CD30L, but not CD30, is expressed on neutrophils. Expression of CD30L can be induced in peripheral blood T cells by cross-linking the CD3 component of the TCR. Peripheral blood T cells exposed to suboptimal concentrations of anti-CD3 increased metabolic activity, proliferated, and produced IL-6 in response to cross-linking of CD30L. These results indicate that cross-linked CD30L can transduce a signal to the ligand-bearing cell. This "reverse signaling" via CD30L taken together with previously published data concerning other ligands in the TNF family strongly suggest that, as a rule, TNF family members and their cognate receptors signal bidirectionally, blurring the distinction between ligand and receptor.
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Dissertations / Theses on the topic "CD30+/CD30L T cell"

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Hirano, Ayumi. "T dependent B cell help in cattle : immunoregulatory function of interleukin-4 and CD40-CD40L interactions /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841150.

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Schubert, Lisa Ann. "Characterization of the transcriptional regulation of the human CD40L gene in CD4 T cells /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/8325.

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Fischer, Marie. "Mast cells in Hodgkin lymphoma : or 'What's a nice cell like you doing in a tumour like this?'." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4620.

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Harlin, Helena. "TRAF4 and CD30/TRAF2 in normal T cell function /." 2001. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3019923.

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Boyle, Julia Katrina. "The role of CD30 in the regulation of T cell function." Thesis, 2003. http://hdl.handle.net/2429/14546.

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CD30 is a member of the TNFR superfamily that was initially identified on Reed-Sternberg cells of Hodgkin's disease and is widely expressed in other lymphomas as well as in a number of autoimmune diseases. On normal cells, CD30 is expressed primarily on activated CD8⁺ T cells and is induced by two distinct pathways, an IL-4 dependent pathway and an IL-4-independent pathway via CD28. The precise role of CD30 has been controversial, but it has been implicated in a number of T cell functions, including costimulation, cytokine production, cell survival and cytotoxicity, although much of the published work to date has been carried out in cell lines. In an attempt to elucidate the role of CD30 in normal T cells, the function of primary lymphocytes derived from CD30-deficient mice was studied. In the absence of CD30, proliferation and activation were normal, with CD30[sup -/-] cells exhibiting levels of proliferation and expression of activation markers comparable to that of wild type cells. As well, among those cytokines examined, production by activated CD30-deficient cells was normal, although production of IL-4 was reduced compared to wild type. 2C-transgenic CD30-deficient cells were unable to kill specific target cells to the same extent as wild type effectors, although expression of effector molecules including perforin, granzyme B and FasL was normal, as was killing of targets when the requirement for TCR recognition was bypassed. Finally, although the reduction of effector function suggested that memory development may also be effected, 2C/CD30[sup -/-] effectors were able to develop into memory-like cells to the same extent as wild type cells. Although the deletion of CD30 has little effect on a number of T cell functions, particularly activation and proliferation, it appears that CD30 does play a role in the regulation of later events such as cytotoxic effector function and the maintenance of IL-4 production.
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Chen, Jui-Chieh, and 陳瑞傑. "The inhibition of T cell proliferation by CD30 expression on the Hodgkin’s cancer cell." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/49838763617401022976.

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碩士<br>國立臺灣大學<br>生物化學暨分子生物學研究所<br>91<br>英文摘要 Hodgkin''s disease is a type of malignant lymphoma, characterized by the presence of abnormal cells, named Reed-Sternberg cells, in patient’s lymph nodes. CD30 was originally described as a marker of Hodgkin/Reed-Sternberg cells. CD30 and its cognate ligand, CD153, belong to members of the TNFR and TNF superfamilies, respectively. CD30 is expressed on the surface of Hodgkin/Reed-Sternberg (H-RS) cell lines (KM-H2), while expression of CD153 can be induced on the surface of peripheral blood T cells by anti-CD3 or PHA activation. In this study, we addressed the effect of CD30 reverse signaling on T cells. By co-cultures of KM-H2 and PBMC activated by anti-CD3 or PHA, we observed T cell proliferation was inhibited. The inhibition was not dependent on cytokines or substances released from KM-H2, because KM-H2 cells were fixed with paraformaldehyde before the co-culture. We further study the effect of CD30 on T cell proliferation with CD30-expressing Chinese Hamster Ovary (CHO) cells to. In the presence of CD30-positive CHO cells, PHA-treated PBMC failed to achieve significant proliferation. Similar effects were observed if PHA-treated PBMC were cultured in the medium containing chimeric CD30-Fc fusion proteins. Taken together, we discover the inhibitory effect of CD30 reverse signaling on CD153-positive T cells. Furthermore, in order to characterize the protein expression profile in response to CD30 reverse signaling, proteomic technology was used. Several candidate spots were found to be likely regulated by CD30 engagement. One of these spots was identified as Mn-SOD by the use of MALDI-TOF MS. We conclude that H-RS cells are able to inhibit the proliferation of activated T cells through the CD30-CD153 interaction, which may lead to a microenvironment in favor of the growth and survival of the tumor cells.
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Snell, Laura Margaret Lucette. "The Role of TNFR Family Members GITR and CD30 on CD8 T Cell Responses." Thesis, 2012. http://hdl.handle.net/1807/36299.

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GITR and CD30 are T cell costimulatory members of the TNFR superfamily known to regulate T cell responses. Elucidating the mechanisms whereby these receptors modulate T cell responses is crucial for maximizing their potential for immunotherapy. In this thesis, I examine the role of GITR and CD30 on CD8 T cell responses to influenza virus. I show that CD8 T cell intrinsic GITR is required for both maximal primary and secondary CD8 T cell expansion to influenza, while in contrast, CD30 is dispensable for anti-influenza CD8 T cell responses. GITR does not impact on CD8 T cell proliferation or homing, however, it mediates CD8 T cell survival signaling. GITR induces TRAF2/TRAF5 dependent, but TRAF1 independent, NF-κB activation, resulting in the upregulation of the pro-survival molecule Bcl-xL. Furthermore, I show that GITR on CD8 T cells can augment viral clearance and confer protection from death upon severe influenza infection of mice. Similarly, CD30 also elicits protection from death upon severe influenza infection, although the cells responsible for this effect remain to be elucidated. In this thesis, I also show that in unimmunized mice GITR expression is upregulated to higher than basal levels on a population of CD8 memory phenotype cells in the bone marrow. In contrast, CD8 memory phenotype T cells in the spleen and LN have GITR levels similar to that on naïve T cells. The upregulation of GITR in the bone marrow is IL-15 dependent and therefore, GITR serves as a marker for cells that have recently received an IL-15 signal. Furthermore, GITR is required for the persistence, but not for the homeostatic proliferation of CD8 memory phenotype T cells in the bone marrow. Therefore, GITR plays a key role for CD8 T cell intrinsic responses to influenza, as well as for the persistence of CD8 memory phenotype T cells.
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"THE CRITICAL ROLE OF CD4+ TH CELLS IN CD8+ CTL RESPONSES AND ANTI-TUMOR IMMUNITY." Thesis, 2012. http://hdl.handle.net/10388/ETD-2012-04-424.

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The goal of this body of research was to elucidate the mechanism by which CD4+ T cells provide help for CD8+ cytotoxic T lymphocyte (CTL) responses in different immunization types. The establishment of diseases, such as chronic infections and cancers, is attributed to severe loss of or dysfunctions of CD4+ T cells. Even in acute infections, CD4+ T cell deficiency leads to poor memory responses. While the role of CD4+ T cells is being increasingly appreciated in these diseases, the timing and nature of CD4+ T help and associated molecular mechanisms are not completely understood. Growing evidence suggests that, depending on the type of infections or immunizations, the requirements of CD4+ T cells can vary for optimal CD8+ CTL responses. In order to understand the modulatory effects of CD4+ T cells for optimal CD8+ CTL responses, two distinct immunization types were chosen. These include: 1) non-inflammatory dendritic cell (DC) immunization, which fails to provide inflammatory/danger signals; and 2) inflammatory adenovirus (AdV) immunization, which provides profound inflammatory/danger signals. This allowed us to study CD4+ T cell’s participation under different inflammatory conditions. The studies described in Chapters 2 and 3 of this thesis were performed to further understand the concept of how CD4+ T cells mediate optimal CD8+ CTL responses. This has been called the “new dynamic model of CD4+ T helper – antigen (Ag)-presenting cells (Th-APCs),” proposed in 2005 by our laboratory. The study described in Chapter 2 shows that Th-APCs participate not only in augmenting CTL-mediated immune responses, perhaps during early phase, but also in regulating cellular immunity, perhaps during a later phase. Through enhanced IL-2, CD80 and CD40L singnaling, and weaker peptideMHC I (pMHC) signaling, Th-APCs stimulated naïve CD8+ T cells to differentiate into effector CTLs, capable of developing into, central memory CTLs. Th-APC-stimulated CD4+ T cells behaved like Th cells in function, augmenting the overall magnitude of CTL responses. In contrast, Th-APCs were able to kill DCs and other Th-APCs, predominantly through perforin-mediated pathway. The experiments described in Chapter 3 revealed a novel co-operative role of cognate Th-CTL interactions, contrary to previously known immune-regulatory mechanisms among Th-Th or CTL-CTL interactions. In our experiments, Th cells, via CD40L, IL-2, and acquired pMHC-I signaling, enhanced CTL survival and transition into functional memory CTLs. Moreover, RT-PCR, flow cytometry and western blot analysis demonstrate that increased survival of Th cell-helped CTLs is matched with enhanced Akt1/NF-κB activation, down-regulation of FasL and TRAIL, and altered expression profiles with up-regulation of prosurvival (Bcl-2) and down-regulation of proapoptotic (NFATc1, Bcl-10, Casp-3, Casp-4, Casp-7) genes/ molecules. Finally, helped CTLs were also able to induce protection against highly metastasizing tumor challenge, explaining why memory CTLs generated under cognate Th1’s help show survival and recall advantages. The studies in Chapter 4 showed how the precursor frequency (PF) of CD8+ T cells impacts CD4+ T helper requirements for functional CTL responses. At endogenous PF, CD4+ T helper signals were necessary for both primary and memory CTL responses. At increased PF, CD4+ T help, and its CD40L but not IL-2 signal became dispensable for primary CTL responses. In contrast, memory CTL responses required CD4+ T cell signals, largely in the form of IL-2 and CD40L. Thus, these results could impact the development of novel immunotherapy against cancers, since their efficacy would be determined in part by CD4+ T help and CD8+ T cell PF. Finally, the study showed the importance of CD4+ T cells for multiple phases of AdV transgene product-specific CTL responses. These include: a) cognate CD4+ T cells enhanced CTL responses via IL-2 and CD40L signaling during primary, maintenance and memory phases; b) polyclonal CD4+ T environment enhanced the survival of AdV-specific CTL survival, partially explaining protracted CTL contraction phase; and c) during the recall phase, the CD4+ T environment, particularly memory CD4+ T cells, considerably enhanced not only helped, but also unhelped, memory CTL expansion. Thus, these results suggest the participation of both cognate and polyclonal CD4+ T cells for multiple phases of AdV-specific CTLs. Taken together, the current work delineated the critical roles of CD4+ T cells in different stages of CTL responses and in the development of anti-tumor immunity. The results presented here will significantly advance our current understanding of immunity to cancers, autoimmunity and chronic infections, since pathogenesis of these diseases is largely determined by CD4+ T helper functions. As most immunization procedures use the principle that is based on functions of memory cells, the knowledge gained from this work will also have a major impact on designing vaccines against intractable diseases, including cancers and chronic infections. Moreover, in advanced tumors, vaccines developed using this knowledge may act synergistically with other cancer treatments such as irradiation, chemotherapy and microsurgery, minimizing their side effects and prolonging the lives of patients.
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Book chapters on the topic "CD30+/CD30L T cell"

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Kadin, Marshall E., and Francine Foss. "Primary Cutaneous and Systemic CD30+ T-cell Lymphoproliferative Disorders." In T-Cell Lymphomas. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-170-7_5.

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Kaudewitz, Peter, Iannis Anagnostopoulos, Michael Hummel, and Harald Stein. "HTLV-1 Proviral Sequences in Cutaneous CD30-Positive T Large Cell Lymphomas." In Basic Mechanisms of Physiologic and Aberrant Lymphoproliferation in the Skin. Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-1861-7_14.

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Kazlouskaya, V., J. Ho, and O. E. Akilov. "Case 42. Primary cutaneous CD30 T-cell posttransplant lymphoproliferative disorder with δ expression." In Cutaneous Lymphomas. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-59129-8_42.

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Wood, G. S., J. W. Gould, and A. C. Gilliam. "Primary cutaneous CD30+ large-cell lymphoma with natural killer-cell phenotype and the t(2;5) translocation." In Cutaneous Lymphomas. Steinkopff, 2001. http://dx.doi.org/10.1007/978-3-642-57624-9_20.

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"CD30+ cutaneous large T-cell lymphoma." In Dermatology Therapy. Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/3-540-29668-9_525.

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Kadin, Marshall E. "Primary Cutaneous CD30-Positive T-Cell Lymphoproliferative Disorders." In Hematopathology. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-7216-0040-6.00039-3.

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"Cd30-Positive Lymphoproliferative Disorders Including Lymphomatoid Papulosis, Borderline Cd30-Positive Lymphoproliferative Disease, Anaplastic Large Cell Lymphoma, and T-Cell-Rich Cd30-Positive Large B Cell Lymphoma." In The Cutaneous Lymphoid Proliferations. John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118776193.ch13.

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"Cd30þ T-cell Lymphoproliferative Disorders Of The Skin." In Cutaneous Lymphomas. CRC Press, 2005. http://dx.doi.org/10.1201/9780849346033-33.

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Conference papers on the topic "CD30+/CD30L T cell"

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Rana, Seema, and Rajiv Tangri. "Anaplastic large cell lymphoma ALK negative vs. peripheral T cell lymphoma (NOS) - diagnostic dilemma." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685354.

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Middle aged female presented with generalised lymphadenopathy and fever for last one month. Peripheral blood findings were within normal limits. There was no extra nodal involvement. FNAC performed initially from a cervical node suggested possibility of Hodgkin’s lymphoma and a whole node biopsy was performed. Histopathogical examination revealed effaced nodal architecture and a polymorphous population of lymphocytes, plasma cells, neutrophils and scattered large mononuclear cells with prominent nucleolus. An initial panel of CD3, CD20, LCA, CD15, CD30 and PAX5 was performed. The large atypical cells were positive for LCA, CD3 and CD30 with variable positivity for CD15. CD 30 showed Golgi and membranous staining. These large atypical cells were negative for PAX5 and CD20. In view of above findings, Hodgkin’s lymphoma was ruled out and a possibility of Non- Hodgkin’s lymphoma was considered. Further IHC markers were performed which included CD2, CD5, CD7, EMA, Alk, CD10 and KI67. CD5 showed variable positivity. The cells of interest were negative for CD2, CD7, ALK and EMA. Ki 67 index was 70-80%. Overall histological and IHC findings favoured Alk negative Anaplastic large cell lymphoma. Differential diagnosis considered was peripheral T cell lymphoma (NOS). Hodgkin’s lymphoma, peripheral T cell lymphoma (NOS) and anaplastic large cell lymphoma share common histomorphological findings. With careful analysis of Immunohistochemistry, it is easier to categorise Hodgkin’s lymphoma. ALK negative anaplastic large cell lymphoma and peripheral T cell lymphoma (NOS) are difficult to categorise and show overlapping features. We in this case have discussed clinical, histomorphological and IHC pattern of Alk negative Anaplastic large cell lymphoma.
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Wu, Yang, Dan Chen, Rong Ma, et al. "Abstract 1444: The new therapy strategy for treatment of peripheral T cell lymphomas: CD30-targeted CAR-modified T cell therapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1444.

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Wu, Yang, Dan Chen, Rong Ma, et al. "Abstract 1444: The new therapy strategy for treatment of peripheral T cell lymphomas: CD30-targeted CAR-modified T cell therapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1444.

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Caires, Elisana Maria Santos, Régis Resende Paulinelli, Miliana Tostes Lucatto, Eneida Ribeiro Marinho, and Henrique Moura de Paula. "BREAST IMPLANT–ASSOCIATED ANAPLASTIC LARGE CELL LYMPHOMA (BIA-ALCL): A CASE REPORT WITH ATYPICAL SYMPTOMS." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2096.

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The BIA-ALCL is a rare type of T-cell lymphoma CD30+ e AKL−, occurring more common in women with Allergantextured implants. It presents most frequently as a late-onset accumulation of seroma fluid between the implant and less frequently as a palpable tumor mass, with malignant cells infiltrating through the capsule and surrounding tissue with potential lymph node and systemic involvement. This article describes a case report of a 65-year-old female patient with BIA-ALCL complaining of erythema in her right breast for almost 7 months. She agreed no family history of cancer and no fever. The patient was diabetic type 2, dyslipidemic, and postmenopausal taking estrogen therapy. She had undergone a breast augmentation with 215 mL polyurethane-coated implants 15 years ago. Imaging revealed right axillary lymph node enlargement, thickening of the breast parenchyma, and minimal periprosthetic seroma. The initial suspicion was infection wherefore she was submitted removal of the implants, partial capsulectomy on the right side, and total contralateral capsulectomy. Immunochemistry confirmed BIA-ALCL CD30+ e AKL− on the right and no disease on the left. Bacterioscopy was negative. A complementary surgical procedure involving removal of all the right capsules, resection of axillary palpable nodes, and reconstruction was necessary to achieve a bilateral oncoplastic mastopexy. The final diagnosis was BIA-ALCL confined capsule with negative margins and none axillary lymph nodes involvement, staging IB. No adjuvant treatment was necessary. The patient remained symptom free during follow-up examinations, and she desires a new breast augmentation.
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Escribà-Garcia, Laura, Carmen Alvarez-Fernández, Ana Carolina Caballero, et al. "Abstract A028: Memory stem T-cells expressing an optimized CD30-specific chimeric antigen receptor (CAR) efficiently eradicate peripheral T-cell lymphoma in vivo." 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-a028.

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Cho, Hyun-Il, Chung-Hyo Kang, Sang-Eun Lee, et al. "250 Chimeric antigen receptors containing CD30-derived costimulatory domain elicit augmented T cell effector functions and anti-tumor efficacy." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0250.

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Heiser, Ryan A., Bryan M. Grogan, Luke S. Manlove, and Shyra J. Gardai. "Abstract 1789: CD30+T regulatory cells, but not CD30+CD8 T cells, are impaired following brentuximab vedotin treatment in vitro and in vivo." 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.am2018-1789.

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Kua, Lindsay, Chee Hoe Ng, Jin Wei Tan, et al. "240 Humanized CD30 chimeric antigen receptor T cells with a novel 4–1BB derived spacer have improved activity and safety against CD30-positive lymphomas." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0240.

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Merz, Christian, Jaromir Sykora, Viola Marschall, et al. "Abstract 1760: The hexavalent CD40 agonist HERA-CD40L augments multi-level crosstalk between T cells and antigen-presenting cells." 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.am2018-1760.

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Kim, Hyemin, Yejin Kim, Jiwon Choi, et al. "Abstract 4074: Direct interaction of CD40 on tumor cell with CD40L on T cells increases the proliferation of tumor cells via the enhancement of TGF-b production and Th17 differentiation." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4074.

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