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Academic literature on the topic 'CD11'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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Journal articles on the topic "CD11"

Escribano, Luis, Alberto Orfao, Jesús Villarrubia, Beatriz Díaz-Agustín, Carlos Cerveró, Agustín Rios, José L. Velasco, Juana Ciudad, José L. Navarro, and Jesús F. San Miguel. "Immunophenotypic Characterization of Human Bone Marrow Mast Cells. A Flow Cytometric Study of Normal and Pathological Bone Marrow Samples." Analytical Cellular Pathology 16, no. 3 (1998): 151–59. http://dx.doi.org/10.1155/1998/341340.

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The goal of the present paper was to define the immunophenotype of bone marrow mast cells (BMMC) from healthy controls and patients with hematologic malignancies (HM) based on the use of multiple stainings with monoclonal antibodies analyzed by flow cytometry. Our results show that BMMC from both groups of individuals display a similar but heterogenous immunophenotype. The overall numbers of BMMC are higher in the HM group of individuals (p= 0.08). Three patterns of antigen expression were detected: (1) markers constantly positive in all cases analyzed (CD9, CD29, CD33, CD43, CD44, CD49d, CD49e, CD51, CD71, CD117, and FcεRI), (2) antigens that were constantly negative (CD1a, CD2, CD3, CD5, CD6, CD11a, CD14, CD15, CD16, CD19, CD20, CD21, CD23, CD25, CD30, CD34, CD38, CD41a, CD42b, CD65, CD66b, HLA-DR, and CD138), and (3) markers that were positive in a variable proportion of cases – CD11b (50%), CD11c (77%), CD13 (40%), CD18 (20%), CD22 (68%), CD35 (27%), CD40 (67%), CD54 (88%) and CD61 (40%). In addition, BMMC from all cases explored were CD45+, and this antigen was expressed at an intensity similar to that of mature granulocytes.In summary, our results show that BMMC from both healthy controls and HM patients display a relatively heterogenous immunophenotype. Interestingly, we have observed clear differences between the immunophenotype of BMMC and MC from other tissues. This could be due either to the heterogeneity of human MC according to their tissue localization or to the sensitivity of the method used for antigen detection.

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Kansas, GS, MJ Muirhead, and MO Dailey. "Expression of the CD11/CD18, leukocyte adhesion molecule 1, and CD44 adhesion molecules during normal myeloid and erythroid differentiation in humans." Blood 76, no. 12 (December 15, 1990): 2483–92. http://dx.doi.org/10.1182/blood.v76.12.2483.2483.

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Abstract We have used three-color flow cytometry to investigate the pattern of expression of the CD11/CD18, CD44, and leukocyte adhesion molecule 1 (LAM-1) adhesion molecules during myeloid and erythroid differentiation in humans. The earliest myeloid cells, identified as CD33loCD15-, were exclusively CD44hi but contained both leukocyte function-associated antigen 1 (LFA-1hi) and LFA-1lo cells, as well as LAM-1+ and LAM-1- cells. This CD33loCD15- myeloid subpopulation expressed only low levels of CD11c and failed to express CD11b, CD14, or any lymphoid (CD3, CD16, CD19) antigens or glycophorin. Commitment to monocyte differentiation, suggested by the presence of an LFA-1hi CD11c+ subset within the CD33loCD15- subpopulation, was clearly signaled by upregulation of CD33; these monocyte-lineage committed cells were exclusively CD33hi, CD44hi, CD11ahi, CD11c+, and exhibited a broad range of intensity of CD15 expression. Later stages of monopoiesis were identified by acquisition of CD11b, and subsequently of CD14. Myeloid cells committed to granulopoiesis remained LFA-1lo, and underwent a sharp upregulation of CD15 along with downregulation of both CD33 and CD44. Successive stages of granulocyte development were marked by expression of CD11b and, subsequently, of CD16. The earliest cells capable of erythroid differentiation were CD44hi, LFA-1lo, and LAM-1+. Both LFA-1 and LAM-1 were lost before the onset of glycophorin (glyco) expression, whereas CD44 expression remained high on glyco+ cells, which also expressed CD45. CD44 expression was intermediate on glyco+ CD71+ cells, and low on glyco+ CD45- CD71- cells, similar to normal, circulating erythrocytes. Our results allow us to phenotypically define discrete stages in the normal development of monocytes, neutrophils, and erythrocytes. The expression of LFA-1, LAM-1, and high levels of CD44 on the most primitive hematopoietic cells detectable by flow cytometry suggests that at least some of these molecules are critically involved in leukocyte adhesion during development.

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We have used three-color flow cytometry to investigate the pattern of expression of the CD11/CD18, CD44, and leukocyte adhesion molecule 1 (LAM-1) adhesion molecules during myeloid and erythroid differentiation in humans. The earliest myeloid cells, identified as CD33loCD15-, were exclusively CD44hi but contained both leukocyte function-associated antigen 1 (LFA-1hi) and LFA-1lo cells, as well as LAM-1+ and LAM-1- cells. This CD33loCD15- myeloid subpopulation expressed only low levels of CD11c and failed to express CD11b, CD14, or any lymphoid (CD3, CD16, CD19) antigens or glycophorin. Commitment to monocyte differentiation, suggested by the presence of an LFA-1hi CD11c+ subset within the CD33loCD15- subpopulation, was clearly signaled by upregulation of CD33; these monocyte-lineage committed cells were exclusively CD33hi, CD44hi, CD11ahi, CD11c+, and exhibited a broad range of intensity of CD15 expression. Later stages of monopoiesis were identified by acquisition of CD11b, and subsequently of CD14. Myeloid cells committed to granulopoiesis remained LFA-1lo, and underwent a sharp upregulation of CD15 along with downregulation of both CD33 and CD44. Successive stages of granulocyte development were marked by expression of CD11b and, subsequently, of CD16. The earliest cells capable of erythroid differentiation were CD44hi, LFA-1lo, and LAM-1+. Both LFA-1 and LAM-1 were lost before the onset of glycophorin (glyco) expression, whereas CD44 expression remained high on glyco+ cells, which also expressed CD45. CD44 expression was intermediate on glyco+ CD71+ cells, and low on glyco+ CD45- CD71- cells, similar to normal, circulating erythrocytes. Our results allow us to phenotypically define discrete stages in the normal development of monocytes, neutrophils, and erythrocytes. The expression of LFA-1, LAM-1, and high levels of CD44 on the most primitive hematopoietic cells detectable by flow cytometry suggests that at least some of these molecules are critically involved in leukocyte adhesion during development.

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Takeshita, Akira, Yukio Murakami, Yoshinori Yamashita, Masami Ishida, Seiichiro Fujisawa, Shigeo Kitano, and Shigemasa Hanazawa. "Porphyromonas gingivalis Fimbriae Use β2Integrin (CD11/CD18) on Mouse Peritoneal Macrophages as a Cellular Receptor, and the CD18 β Chain Plays a Functional Role in Fimbrial Signaling." Infection and Immunity 66, no. 9 (September 1, 1998): 4056–60. http://dx.doi.org/10.1128/iai.66.9.4056-4060.1998.

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ABSTRACT In this study, we demonstrate that Porphyromonas gingivalis fimbriae use molecules of β2 integrin (CD11/CD18) on mouse peritoneal macrophages as cellular receptors and also show that the β chain (CD18) may play a functional role in signalling for the fimbria-induced expression of interleukin-1β (IL-1β) and tumor necrosis factor alpha (TNF-α) genes in the cells. Using a binding assay with 125I-labeled fimbriae, we observed that fimbrial binding to the macrophages was inhibited by treatment with CD11a, CD11b, CD11c, or CD18 antibody but not by that with CD29 antibody. Western blot assays showed that the fimbriae bound to molecules of β2 integrin (CD11/CD18) on the macrophages. Furthermore, Northern blot analyses showed that the fimbria-induced expression of IL-1β and TNF-α genes in the cells was inhibited strongly by CD18 antibody treatment and slightly by CD11a, CD11b, or CD11c antibody treatment. Interestingly, intracellular adhesion molecule 1 (ICAM-1), a ligand of CD11/CD18, inhibited fimbrial binding to the cells in a dose-dependent manner. In addition, ICAM-1 clearly inhibited the fimbria-induced expression of IL-1β and TNF-α genes in the cells. However, such inhibitory action was not observed with laminin treatment. These results suggest the importance of β2 integrin (CD11/CD18) as a cellular receptor ofP. gingivalis fimbriae in the initiation stage of the pathogenic mechanism of the organism in periodontal disease.

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Lunghi, Monia, Laura Vanelli, Paolo Bernasconi, Marina Boni, Monica Portolan, Cristiana Pascutto, Alessandra Algarotti, Vassiliky Griva, Carlo Castagnola, and Mario Lazzarino. "The Relationship between the Immunophenotypic Profile and Cytogenetic Abnormalities in Acute Myeloid Leukemia." Blood 106, no. 11 (November 16, 2005): 4495. http://dx.doi.org/10.1182/blood.v106.11.4495.4495.

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Abstract We studied the immunophenotypic characteristics of 459 consecutive adult AML patients and their correlation with karyotype. Immunophenotype was performed using a panel of 26 directly conjugated monoclonal antibodies. Cytogenetic analysis was performed using a standard G-banding technique. Karyotype was available in 394 patients (not done in 15, failed in 50): 1) 45 (11.4%) were t(15;17) APL patients with a mature myeloid phenotype (HLA-DR-/CD13+ and/or CD33+). CD2 and CD56 were expressed in 20% and 13.3% of cases, respectively. CD11b-positivity was less frequent than in the other cytogenetic groups. The markers significantly associated with t(15;17) were: presence of CD2 (two tailed Fisher exact test: p=.003) and CD117 (p=.01), absence of CD4dim (p<.001), CD7 (p<.001), CD11b (p<.001), CD11c (p<.001), CD14 (p<.001), CD34 (p<.001), TdT (p=.03) and HLA-DR (p<.001). 2) 12 (3%) showed t(8;21) and were characterized by CD34+/CD19+/CD13+<CD33+ in more than 80% of blasts. CD56 were expressed in 87.5%. CD11b was positive only in 8.3% and CD14 was constantly negative. In univariate analysis, t(8;21) was associated with CD11b- (p=.03), CD19+ (p<.001) and CD56+(p<.001). 3) 23 (5.8%) had inv(16) or t(16;16) with CD13+/CD33+ in >90% of blasts, CD34+ in 70%, MPO+ in 95.8% and HLA-DR+ in 89.3%. The association with CD14 and TdT was of borderline statistical significance. 4) 24 (6.1%) had −5/5q- with more than 80% of blasts CD117+/CD13+>CD33+. CD34 was positive in 62.9% of cases, CD7 in 33%, CD11b in 35.7%, CD11c in 67.8% and CD14 in 7.1%. CD15-positivity was less frequent than in other AML subtypes. Univariate analysis showed a trend of positive association with CD7 and CD117. 5) 40 (10.2%) showed −7/7q-, with CD13+>CD33+ detected in more than 80%, CD7 in 33.3%, CD11b in 72.7%, CD15 in 55%, CD34 in 73.3%. Abnormal CD16/CD33 and/or CD11b/CD66b myeloid cell pattern was detected in 40% of cases (p=.001). −7/7q- were significantly associated with CD34 (p=.02) and CD7 (p=.04). 6) 41 (10.4%), had complex karyotype (≥3 abn) with a similar antigenic profile than group 4) and 5) but with a more frequent expression of CD11b, CD14, CD15 and less frequent of MPO. In univariate analysis CD19 (p=.04), CD34 (p=.02) and MPO (p<.001) retained statistical significance. 7) 20 (5.1%) with +8 were CD13+ in 95.6%, while the other markers were present in less than 80% of cases, in particular lower CD33+ blasts (p=.01). 8) 17 (4.3%) had 11q23abn, with CD13+<CD33+, frequent TdT+ (61.5%) and rare CD34+ (31.8%, p=.02). CD11c and CD14 were more frequently expressed than in other subtypes (86.4% and 36.4%, respectively). T-lymphoid markers were present in 36.4%. Univariate analysis showed a positive association between 11q23abn and presence of CD11c (p=.04) and CD14 (p=.05). 9) 115 (29.2%) with a normal karyotype had a dishomogeneous antigenic profile. CD2 (p=.002), CD11c (p=.04) and HLA-DR (p<.001) were the most discriminant markers. Using a multivariate discriminant analysis, we identified a discriminant function only for group 1) and group 2), based on CD11c/CD13/CD34/MPO/HLA-DR (sensitivity >99%, specificity 94.7%) and CD7/CD11c/CD19/CD56/MPO/HLA-DR (sensitivity 83.3%, specificity 94.5%), respectively. We conclude that in AML patients some cytogenetic abnormalities are associated with peculiar antigenic profiles. In patients with normal karyotype the heterogeneity of antigenic pattern may reflect underlined distinct molecular abnormalities.

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Lee, S. H., P. R. Crocker, S. Westaby, N. Key, D. Y. Mason, S. Gordon, and D. J. Weatherall. "Isolation and immunocytochemical characterization of human bone marrow stromal macrophages in hemopoietic clusters." Journal of Experimental Medicine 168, no. 3 (September 1, 1988): 1193–98. http://dx.doi.org/10.1084/jem.168.3.1193.

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Stromal macrophages (M phi) have been localized in situ and isolated within erythroid clusters from human marrow. Stromal M phi arborize in an extensive network uniformly distributed throughout marrow interstitium, and express the phenotype CD4+, CD11a+, CD11c+, CD13+, CD14+, CD16+, CD18+, CD31+, CD32+, FcRI+, HLA-DR+, and CD35-, transferrin receptor-negative, and CD11b (weak). They express endocytic receptor antigens, but show significant differences in myeloid antigen expression compared with freshly harvested or cultured monocytes. Human stromal M phi are therefore specialized mature marrow M phi that are accessible for further investigations in infectious, storage, or hemopoietic disorders.

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Bradstock, K., J. Matthews, E. Benson, F. Page, and J. Bishop. "Prognostic value of immunophenotyping in acute myeloid leukemia. Australian Leukaemia Study Group." Blood 84, no. 4 (August 15, 1994): 1220–25. http://dx.doi.org/10.1182/blood.v84.4.1220.1220.

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Abstract The diagnostic and prognostic value of immunophenotyping with 18 murine monoclonal antibodies (MoAbs) to a variety of leukocyte differentiation antigens was assessed in 168 adults aged 15 to 60 years with acute myeloid leukemia (AML). Patients were entered on the multicentre Australian Leukaemia Study Group M4 protocol, and were randomized to receive either standard or high-dose Ara-C together with daunorubicin and etoposide as induction chemotherapy, followed by standard consolidation and maintenance therapy. Diagnostic bone marrow aspirate (152 cases) or peripheral blood samples (16) were analyzed by indirect immunofluorescence and flow cytometry. MoAbs used were directed at myeloid (CD11b, CD13, CD14, CD15, CD33, CD41), lymphoid (CD2, CD3, CD7, CD9, CD10, CD19), or stem cell (HLA-DR, CD34, c-kit receptor) antigens, as well as the leukocyte integrins CD18 and CD49e, and the transferrin receptor CD71. Of the myeloid markers, CD13 and CD33 were the most useful diagnostically (71% and 79% of cases positive, respectively), with CD11b, CD14, and CD15 less commonly positive. A minority of cases expressed lymphoid antigens, either T cell (CD2 16%, CD3 7%, CD7 28%) or B cell (CD10 2%, CD19 7%). CD34 was detected on 42% and c-kit receptor on 48%. When patients were analyzed for response to treatment, CD2, CD9, and CD14 were significantly associated with complete remission rate: cases expressing these antigens had a poorer response than negative cases. In univariate analysis, CD11b+ cases had shorter periods of remission (relative risk of relapse, 2.33; P = .003) and shorter survival (relative death rate, 1.91; P = .006). In multivariate analysis, adjusting for other prognostic factors, CD9 and CD11b were significantly predictive of shorter survival. No other marker had a significant predictive effect. We conclude that myeloid MoAbs are useful in confirming the diagnosis of AML, but their prognostic value may be limited to CD11b. Lymphoid antigen expression is a consistent phenomenon in a minority of cases of AML, but appears to have little clinical significance.

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The diagnostic and prognostic value of immunophenotyping with 18 murine monoclonal antibodies (MoAbs) to a variety of leukocyte differentiation antigens was assessed in 168 adults aged 15 to 60 years with acute myeloid leukemia (AML). Patients were entered on the multicentre Australian Leukaemia Study Group M4 protocol, and were randomized to receive either standard or high-dose Ara-C together with daunorubicin and etoposide as induction chemotherapy, followed by standard consolidation and maintenance therapy. Diagnostic bone marrow aspirate (152 cases) or peripheral blood samples (16) were analyzed by indirect immunofluorescence and flow cytometry. MoAbs used were directed at myeloid (CD11b, CD13, CD14, CD15, CD33, CD41), lymphoid (CD2, CD3, CD7, CD9, CD10, CD19), or stem cell (HLA-DR, CD34, c-kit receptor) antigens, as well as the leukocyte integrins CD18 and CD49e, and the transferrin receptor CD71. Of the myeloid markers, CD13 and CD33 were the most useful diagnostically (71% and 79% of cases positive, respectively), with CD11b, CD14, and CD15 less commonly positive. A minority of cases expressed lymphoid antigens, either T cell (CD2 16%, CD3 7%, CD7 28%) or B cell (CD10 2%, CD19 7%). CD34 was detected on 42% and c-kit receptor on 48%. When patients were analyzed for response to treatment, CD2, CD9, and CD14 were significantly associated with complete remission rate: cases expressing these antigens had a poorer response than negative cases. In univariate analysis, CD11b+ cases had shorter periods of remission (relative risk of relapse, 2.33; P = .003) and shorter survival (relative death rate, 1.91; P = .006). In multivariate analysis, adjusting for other prognostic factors, CD9 and CD11b were significantly predictive of shorter survival. No other marker had a significant predictive effect. We conclude that myeloid MoAbs are useful in confirming the diagnosis of AML, but their prognostic value may be limited to CD11b. Lymphoid antigen expression is a consistent phenomenon in a minority of cases of AML, but appears to have little clinical significance.

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Gorczyca, Wojciech, Henry Dong, James Weisberger, and Zach Liu. "Hypergranular Non-M3 Acute Myelogenous Leukemia: A Potential Pitfall in Flow Cytometric Diagnosis." Blood 104, no. 11 (November 16, 2004): 4452. http://dx.doi.org/10.1182/blood.v104.11.4452.4452.

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Abstract Background Flow cytometry (FC) is an important tool in the diagnosis, subclassification and clinical management of acute leukemias. CD45 vs. orthogonal or side scatter (SSC) gating criteria allows easy identification of non-M3 blasts, which form a coherent population in the low SSC/moderate CD45 blast gate. The vast majority of acute myeloid leukemias (AML) of non-M3 type express pan-myeloid antigens CD13 and CD33, HLA-DR, blastic markers CD34 and CD117. AML M3 (acute promyelocytic leukemia, APL) often lacks CD34 and HLA-DR expression, and has characteristically high SSC/moderate CD45 expression, which overlaps with the granulocyte gate, but is CD117-positive. We report nine cases of non-M3 AML (hypergranular AML) with increased side scatter, moderate CD45 expression, and lack of expression of blastic markers, which mimic APL. Design Multiparameter 4-color FC analysis was performed on peripheral blood and/or bone marrow aspirate samples using the following antibody panel: CD2, CD3, CD4, CD5, CD7, CD8, CD10, CD11b, CD11c, CD13, CD14, CD16, CD19, CD20, CD33, CD34, CD38, CD45, CD56, CD64, CD79a, CD117, TdT, and HLA-DR. Fresh bone marrow aspirate and/or peripheral blood films and cytospin preparations from FC samples were stained with Wright Giemsa and reviewed in each case. Results Instead of a coherent population of blasts in the low SSC/moderate CD45 blast gate, the blasts in all 9 cases displayed increased granularity, which placed them in the granulocyte gate on FC display. The immunophenotype was as follows: HLA-DR+ in 5/9, CD4+ in 6/9, CD10+ in 1/9, CD11b+ in 4/9, CD11c+ in 8/9, CD13+ in 8/9, CD14+ in 0/9, CD16+ in 0/9, CD19+ in 0/9, CD33+ in 9/9, CD34+ in 0/9, CD38+ in 9/9, CD56+ in 5/9, CD64+ in 9/9 and CD117+ in 0/9 cases. The cytologic preparations revealed type II and type III cytomorphology in all 9 cases; none contained Auer rods. Conclusion Hypergranular non-M3 AML is difficult to diagnose by FC by pattern recognition because the blasts overlap with maturing granulocytes by SSC/CD45 gating criteria, and are not located in the blast gate. In this respect, they mimic APL and regenerative marrows, including those following G-CSF therapy. Correlation with cytomorphology and the expression of CD10, CD11b, CD16 and CD56 helps to differentiate between hypergranular AML, benign processes, APL, and MDS. Specifically, benign maturing myeloid cells show graduating positivity for CD10, CD11b and CD16, and are negative for CD56. This is the inverse pattern of the majority of cases of hypergranular AML. These cases differ from APL by expression of HLA-DR (in a majority of cases), lack of CD117, and different cytomorphology. Myelodysplastic syndromes, which may display similar aberrant myeloid expression of CD10, CD11b, CD16 and CD56, are most often low in SSC, and blastic cells will be <20% cytologically on smear review.

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Chatila, T. A., R. S. Geha, and M. A. Arnaout. "Constitutive and stimulus-induced phosphorylation of CD11/CD18 leukocyte adhesion molecules." Journal of Cell Biology 109, no. 6 (December 1, 1989): 3435–44. http://dx.doi.org/10.1083/jcb.109.6.3435.

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The leukocyte CD11/CD18 adhesion molecules (beta 2 integrins) are a family of three heterodimeric glycoproteins each with a distinct alpha subunit (CD11a, b, or c) and a common beta subunit (CD18). CD11/CD18 mediate crucial leukocyte adhesion functions such as chemotaxis, phagocytosis, adhesion to endothelium, aggregation, and cell-mediated cytotoxicity. The enhanced cell adhesion observed upon activation of leukocytes is associated with increased surface membrane expression of CD11/CD18, as well as a qualitative upregulation of CD11/CD18 functions. To elucidate the nature of the qualitative modifications that occur, we examined the phosphorylation status of these molecules in resting human leukocytes and upon activation with PMA or with the chemotactic peptide F-met-leu-phe (FMLP). In unstimulated cells, all three CD11 subunits were found to be constitutively phosphorylated. In contrast, phosphorylation of the common CD18 subunit was minimal. PMA induced rapid and sustained phosphorylation of CD18 that occurred at high stoichiometry, but had only minimal effects on phosphorylation of the associated CD11 subunits. FMLP also induced rapid phosphorylation of CD18, but the effect was of short duration. FMLP-induced phosphorylation of CD18 was not related to its Ca++-mobilizing effect, as CD18 phosphorylation was not observed upon treatment of leukocytes with the Ca++ ionophore, ionomycin. Phosphoamino acid analysis of CD11/CD18 in PMA- or FMLP-treated monocytes revealed a predominance of phosphoserine residues in all CD11/CD18 subunits. A small component of phosphothreonine was present in CD11c and CD18 and a minor component of phosphotyrosine was also detected in CD18 upon leukocyte activation may regulate the adhesion functions mediated by the CD11/CD18 family of molecules.

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Dissertations / Theses on the topic "CD11"

Johansson, Joakim, Florence Sjögren, Mikael Bodelsson, and Folke Sjöberg. "Dynamics of leukocyte receptors after severe burns: An exploratory study." Linköpings universitet, Hälsouniversitetet, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-67169.

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Background: Patients with burns are susceptible to organ failure, and there is indirect evidence that leukocytes may contribute to this process. They may change the expression of cell-surface receptors after certain stimuli, for example, the burn. We therefore aimed to assess the changes induced by the burn in the expression of leukocyte cell-surface receptors CD11b, CD14, CD16, and CD62L on the surface of PMNs and monocytes. We also wanted to examine the dynamics of this activation during the first week after the burn, and to relate it to the size of the injury. Methods: Ten patients with burns of andgt;15% (TBSA) were included in the study. Blood samples were collected on arrival and every consecutive morning during the first week. Healthy volunteers acted as controls. Results: PMN CD11b expression was increased. The extent of PMN CD11b expression correlated negatively to the size of the full thickness burn. Monocyte CD14 expression increased initially but there was no relation to the size of the burn. PMN CD16 expression decreased initially during the first days and the decrease was related to burn size. CD62L did not vary depending on the burn in either PMN or monocytes during the first week after the burn. Conclusion: This study showed that specific receptors on the surface of leukocytes (PMN CD11b, monocyte CD14 and PMN CD16) are affected by the burn. Expression of PMN CD11b and CD16 are related to burn size. Burn-induced effects on the expression of PMN receptors, such as PMN CD11b and CD16, may contribute to burn-induced infection susceptibility.
Original Publication: Joakim Johansson, Florence Sjögren, Mikael Bodelsson and Folke Sjöberg, Dynamics of leukocyte receptors after severe burns: An exploratory study, 2011, BURNS, (37), 2, 227-233. http://dx.doi.org/10.1016/j.burns.2010.08.015 Copyright: Elsevier Science B.V., Amsterdam. http://www.elsevier.com/

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Daniels, Brodie Belinda. "Molecular and cellular analysis of the interaction between soluble CD23 and CD11/CD18 integrins." Thesis, Nelson Mandela Metropolitan University, 2010. http://hdl.handle.net/10948/1217.

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The low affinity IgE receptor, CD23, is expressed by a wide variety of cells and cleaved from its original 45 kDa size to several smaller soluble CD23 proteins. Soluble CD23 function depends on the form of the protein and its interaction with various ligands. CD23 is believed to play an important role in regulating allergic responses and in inflammation, amongst others. β2 integrins are important in a variety of cell-adhesion reactions during immune-inflammatory mechanisms and the binding of their natural ligands generates outside-in cellular signalling, leading to cell activation. Although the binding of CD23 to β2 integrins contributes to this signalling in monocytes, the interaction site for CD23 is unknown. This study focused on the interaction of three soluble CD23 proteins with the β2 integrins CD11b/CD18 and CD11c/CD18. Differentiated HL60, THP1 and U937 monocytic cells were used to demonstrate the binding of three recombinant CD23 constructs (corresponding to 16, 25 and 33 kDa human soluble CD23) to upregulated CD11b/CD18 and CD11c/CD18. This binding was partially blocked by an antibody specific for the CD11b/CD18 αI domain, demonstrating that αI domains are involved in binding to CD23. Recombinant αI domain proteins of CD11b and CD11c were demonstrated to bind CD23 using ELISA and in surface plasmon resonance spectroscopy. The dissociation constants for CD23-CD11b/CD18 and CD23-CD11c/CD18 are comparable to other integrin ligands. This study has shown that CD23 interacts directly with the αI domains of β2 integrins and that the interaction surface likely spans the lectin domain as well as either the stalk and/or C-terminal tail of CD23. This study also looked at the effect that soluble CD23 proteins had on monocyte biology. It appears that iv sCD23 proteins have little effect on the phagocytic or chemotactic ability of monocytes, while an increase in oxidative burst was shown with the 16 kDa and 25 kDa CD23 proteins. Signalling pathways for the production of reactive oxygen species were investigated and it appears that the CD23 proteins signal mainly through the phosphoinositide-3 kinase pathway, although the mitogen activated protein kinase and Src kinase pathways may also play a role. These data suggest that sCD23 proteins induce outside-in signalling of β2 integrins and are able to change the activation state of CD11b/CD11c by stimulating oxidative burst. This needs to be further investigated by determining how the three sCD23 proteins are binding the CD11 proteins and investigating further leukocyte function and inflammatory responses by the cells.

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Fagerholm, Susanna. "Bidirectional signalling and phosphorylation of CD11 /." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/fagerholm/.

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Faulhaber, Fabrízia Rennó Sodero. "Expressão de marcadores de superfície de neutrófilos em recém nascidos ictéricos antes e após a fototerapia." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/179819.

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A icterícia por hiperbilirrubinemia indireta afeta mais de 60% dos recém-nascidos a termo. O tratamento, quando necessário, é realizado através da fototerapia. Não existem estudos na literatura avaliando os efeitos da fototerapia na função dos neutrófilos de recém-nascidos. O melhor entendimento da função dos neutrófilos nos recém-nascidos antes e após a fototerapia seria importante para avaliar as possíveis repercussões na expressão dos neutrófilos desencadeadas pelo tratamento fototerápico. O objetivo deste estudo foi avaliar e comparar a função dos neutrófilos, através da mensuração pela citometria de fluxo da expressão dos principais marcadores de superfície em recémnascidos ictéricos, antes e após 24 horas de fototerapia. Metodologia: Foram incluídos recém-nascidos com idade gestacional ≥ 35 semanas e peso de nascimento ≥ 2000g, que possuiam critérios da Academia Americana de Pediatria para tratamento fototerápico. Os critérios de exclusão foram: mal-formações congênitas, síndromes com alterações cromossômicas, erro inato do metabolismo, infecções do grupo STORCH, asfixia neonatal, sepse ou suspeita de sepse, exsanguineotransfusão, transfusão de hemocomponentes e uso de imunoglobulina. Foi realizada a avaliação de expressão da intensidade média de fluorescência (IMF) de CD10, CD11b, CD11c, CD15, CD16, CD18, CD62L, CD64 e CD66, antes do início e após 24 horas do início da fototerapia. Foram utilizados o teste T de Student para análise dos dados. Resultados: Foram incluídos 25 recém-nascidos no estudo, com idade mediana de 53 (27.5-75.5) horas de vida e bilirrubina média de 13.6±2.85 mg/dL. Não houve diferença estatística na expressão de CD11b, CD15, CD18, CD62L, CD64 e percentual de neutrófilos antes e após 24 horas de fototerapia. Ocorreu aumento da expressão de CD10 8 (p=0.038) e CD16 (p=0.017) e redução da expressão de CD11c (p=0.023) e CD66acde (p=0.004) após 24 horas de fototerapia. Conclusão: Os recém-nascidos submetidos ao tratamento fototerápico apresentaram aumento da expressão de CD10 e de CD16 e diminuição da expressão de CD11c e de CD66acde após 24 horas de exposição, que pode estar relacionado a um efeito antiinflamatório da fototerapia nos recém-nascidos expostos a este tratamento.
Jaundice due to indirect hyperbilirubinemia affects more than 60% of term neonates. The treatment when necessary is carried out using phototherapy. There are no studies in the literature evaluating the effect of phototherapy on the function of neonates' neutrophils. A better understanding of the function of neutrophils in neonates before and after phototherapy would be important in order to assess potential effects on the expression of neutrofils triggered by the phototherapy treatment. The aim of this study was to assess and compare the function of neutrophils by measuring the expression of the main surface markers in icteric neonates, using flow cytometry, before and after 24 hours of phototherapy. Methodology: Neonates at a gestational age ≥ 35 weeks and at a birth weight ≥ 2000g who met the criteria of the American Academy of Pediatrics for phototherapy were included. The exclusion criteria were: congenital malformations, syndromes with chromosomal alterations, inborn errors of metabolism, infections of the STORCH group, neonatal asphyxia, sepsis or suspicion of sepsis, exchange transfusion, transfusion of blood components, and use of immunoglobulin. The evaluation of the MFI expression of CD10, CD11b, CD11c, CD15, CD16, CD18, CD62L, CD64 and CD66 was performed before and 24 hours after the initiation of phototherapy. The chi-square and Student T tests were used for data analysis. Results: Twenty-five neonates were included in the study at the mean age of 53 (27.5- 75.5) hours of life and with a mean bilirubin level of 13.6±2.85 mg/dL. There was no statistical difference in the expression of CD11b, CD15, CD18, CD62L, CD64 and percentage of neutrophils before and after 24 hours of phototherapy. There was an increase in the expression of CD10 (p=0.038) and CD16 (p=0.017) and a reduction in 10 the expression of CD11c (p=0.023) and CD66acde (p=0.004) after 24 hours of phototherapy. Conclusion: The newborns submitted to phototherapy had increased expression of CD10 and CD16 and decreased expression of CD11c and CD66acde after 24 hours of exposure, which may be related to an anti-inflammatory effect of phototherapy on the neonates exposed to this treatment.

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Owen, Caroline Ann. "Monocyte adherence to fibronectin : role of CD11/CD18 integrins and relationship to other monocyte functions." Thesis, University of Birmingham, 1993. http://etheses.bham.ac.uk//id/eprint/36/.

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Regulated adherence of monocytes to extracellular matrix macromolecules is a prerequisite for their accumulation at sites of pulmonary infection and inflammation. To begin to assess the pathobiological importance of alterations in monocyte adherence to extracellular matrix in inflammatory lung diseases, the adherence properties of monocytes from patients with an inflammatory lung disease (bronchiectasis) and healthy subjects to a representative matrix component (fibronectin) were compared. Spontaneous adherence of monocytes from the control subjects was 20 to 25%, whereas that of the patients' cells was 2 to 3-fold higher and correlated with the severity of airway inflammation. Endotoxin (LPS) and cytokines from areas of airway disease are likely to be responsible for the observed monocyte activation since: 1) LPS was detected in plasma from all of the patients but none of the control subjects; and 2) LPS and cytokines produced dose-related increases in the adherence of normal monocytes in vitro. Monocyte adherence to fibronectin was substantially mediated by CD11/CD18 integrins, via both RGD-dependent and RGD-independent mechanisms. These data indicate that signals arising from foci of pulmonary inflammation are likely determinants of the accumulation of monocytes in the lungs of patients with chronic inflammatory lung diseases. There was a striking relationship between the adherence properties of monocytes and functions that are of biological importance at sites of inflammation. Spontaneously adherent monocytes had an "inflammatory effector" phenotype, non-adherent cells had an "immune modulatory" phenotype and monocytes that could stimulated to adhere by LPS (LPS-adherent cells) had an intermediate phenotype. In addition, only the adherent monocyte subpopulations were replete with HLE and these cells contained a substantial (10 to 11-fold) molar excess of HLE compared with the physiological inhibitor of this enzyme (a1-antitrypsin). Maturation in vitro increased the accumulation of a1-antitrypsin by all of the monocyte subpopulations. In contrast, proinflammatory mediators up-regulated a1-antitrypsin accumulation by only the spontaneously adherent cells, probably by translational or post-translational mechanisms. In conclusion, these data indicate that monocytes are heterogeneous in their ability to accumulate at sites of infection and inflammation. In addition, the capacity of monocytes to adhere to fibronectin is related to monocyte functions that are of biological importance at sites of infection and inflammation. Furthermore, LPS released from foci of infection, may induce the accumulation of monocytes with an inflammatory effector phenotype, and may thereby promote resolution of tissue infection. Alternatively, LPS may promote the recruitment of monocytes with capacity to contribute to HLE-mediated tissue injury.

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Baj, Agnes [Verfasser]. "Polymorphismen im CD11-Cluster bei Patienten mit Koronarer Herzerkrankung / Agnes Baj." Kiel : Universitätsbibliothek Kiel, 2011. http://d-nb.info/1020202610/34.

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Sloma, Ivan. "Biologie des protéines CD1a, CD1b et CD1c : De l'expression monocytaire à la présentation de l'antigène par les cellules dendritiques." Paris 5, 2007. http://www.theses.fr/2007PA05D036.

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Les protéines CD1a, CD1b et CD1c sont des molécules non classiques de présentation de l'antigène. Leur structure est analogue à celle des protéines du complexe majeur d'histocompatibilité de classe I. Exprimées par les cellules dendritiques, elles présentent des antigènes lipidiques à des lymphocytes T spécifiques qui vont participer aux réponses immunes anti-infectieuses et anti-tumorales. Après un rappel de l'état des connaissances sur les protéines CD1 du groupe I et les cellules dendritiques, ce manuscrit présente tout d'abord les résultats de trois études s'intéressant à l'expression monocytaire des protéines CD1 dans la drépanocytose et sa relation avec la susceptibilité aux infections bactériennes. Dans un deuxième temps sont développées les études de l'organisation membranaire de la protéine CD1a, son impact sur l'activation lymphocytaire T et l'implication de CD1a dans l'induction d'un signal de maturation de la cellule dendritique
CD1a, CD1b and CD1c proteins are non classical MHC-class I antigen presenting molecules. They display structural homology with MHC-class I proteins. Expressed on dendritic cells, they present glycolipid antigens to specific T lymphocytes with participate to anti-infectious and anti-tumoral immune responses. After an extensive review on CD1 antigen presenting system and dendritic cell populations, this manuscript presents firstly three studies on CD1 expression on monocytes in sickle cell disease and its relation with susceptibility towards severe bacterial infection. In a second part data on CD1a membrane organization and its impact on T cell activation and dendritic cell maturation are presented

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Welcker, Silvia. "Selektion konformationsspezifischer Aptamere sowohl gegen das aktivierte Leukozytenintegrin Mac-1 (alphaM beta 2, CD11b, CD18) als auch gegen den nicht aktivierten und aktivierten Integrin-Rezeptor alphaV Beta 3 (Vitronektin-Rezeptor, CD51,CD61)." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:25-opus-44251.

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Pyszniak, Andrew M. "Regulation of LFA-1 (CD11a/CD18) function." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq25139.pdf.

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Wohler, Jillian E. "The role of the [beta]₂-integrin family on T cell subsets." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009p/wohler.pdf.

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Books on the topic "CD11"

Owen, Caroline A. Monocyte adherence to fibronectin: Role of CD11/CD18 integrins and relationship to other monocyte functions. Birmingham: University of Birmingham, 1992.

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Moody, D. Branch, ed. T Cell Activation by CD1 and Lipid Antigens. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-69511-0.

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name, No. Ectopeptidases: CD13/aminopeptidase N and CD26/dipeptidylpeptidase IV in medicine and biology. New York, NY: Kluwer Academic/Plenum, 2003.

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Pumphrey, Nicholas Jonathan. Delineating the signalling potential of the cytoplasmic tail of CD31, and related protein CD66a. Birmingham: University of Birmingham, 2000.

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Roger, Knowles. Better by design?: A contractor's guide to the JCT standard form of buildingcontract with contractor's design (CD81). Knutsford: Knowles, 1990.

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David, Chappell, and Smith Mark, eds. Better by design?: A contractor's guide to the JCT standard form of building contract with contractor's design (CD81). 2nd ed. Knutsford: Knowles Publications, 1994.

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S, Jack Robert, ed. CD14 in the inflammatory response. Basel: Karger, 2000.

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Computer arts: CD101 : October 2004. Future, 2004.

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Jack, R. S., ed. CD14 in the Inflammatory Response. S. Karger AG, 1999. http://dx.doi.org/10.1159/isbn.978-3-318-00463-2.

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Bowen, P. Ellis M. Way Ahead 1 Tb Cdx1. Macmillan, 2010.

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Book chapters on the topic "CD11"

Van Rhijn, Ildiko, Dalam Ly, and D. Branch Moody. "CD1a, CD1b, and CD1c in Immunity Against Mycobacteria." In Advances in Experimental Medicine and Biology, 181–97. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6111-1_10.

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Schmidt, Jan, E. Ryschich, H. Mayer, M. M. Gebhard, Ch Herfarth, and E. Klar. "Fehlende Stimulierbarkeit der CD11 b/CD18-vermittelten Leukozytenadhäsion durch Platelet-Activating-Faktor (PAF) und f-MLP im malignen Tumorendothel beim experimentellen Pankreaskarzinom der Ratte." In Chirurgisches Forum ’98, 413–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72182-3_89.

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van Zelm, Menno C., and Ismail Reisli. "CD19 Deficiency Due to Genetic Defects in the CD19 and CD81 Genes." In Encyclopedia of Medical Immunology, 1–12. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-9209-2_24-1.

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van Zelm, Menno C., and Ismail Reisli. "CD19 Deficiency due to Genetic Defects in the CD19 and CD81 Genes." In Humoral Primary Immunodeficiencies, 83–95. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91785-6_7.

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van Zelm, Menno C., and Ismail Reisli. "CD19 Deficiency Due to Genetic Defects in the CD19 and CD81 Genes." In Encyclopedia of Medical Immunology, 123–34. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_24.

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Carter, R. H., and R. A. Barrington. "Signaling by the CD19/CD21 Complex on B Cells." In Current Directions in Autoimmunity, 4–32. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000075685.

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Dana, Nava, Dehmani M. Fathallah, and M. Amin Arnaout. "Function of a Soluble Human β2 Integrin CD11b/CD18." In Structure, Function, and Regulation of Molecules Involved in Leukocyte Adhesion, 34–44. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9266-8_4.

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Hughes, B. J., J. C. Hollers, and C. Wayne Smith. "Mac-1 (CD11b/CD18) and Adherence-Dependent Neutrophil Locomotion." In Structure, Function, and Regulation of Molecules Involved in Leukocyte Adhesion, 45–57. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9266-8_5.

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Nielsen, Gitte Krogh, and Thomas Vorup-Jensen. "Detection of Soluble CR3 (CD11b/CD18) by Time-Resolved Immunofluorometry." In The Complement System, 355–64. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-724-2_30.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CD91." In Encyclopedia of Signaling Molecules, 359–64. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_413.

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Conference papers on the topic "CD11"

Mukherjee, Kalyan K., Debasish Banerjee, Anjan Das, Subham Halder, Dattatreya Mukherjee, Shyam S. Mondal, Surya K. Roy, Mili Das, Chinmay K. Panda, and Utpal Chaudhuri. "Significance of Detecting Minimal Residual Disease by Flow Cytometry and its Impact on Overall Survival and Prognosis of Pediatric B-Cell ALL Patient Experience from a Tertiary Care Centre in Eastern India." In Annual Conference of Indian Society of Medical and Paediatric Oncology (ISMPO). Thieme Medical and Scientific Publishers Pvt. Ltd., 2021. http://dx.doi.org/10.1055/s-0041-1735366.

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Abstract Introduction The improved prognosis of pediatric B-cell acute lymphoblastic leukemia (pBALL) is considered as a good progress of medical science in the field of oncology and hematology. Minimal residual disease (MRD) refers to presence of disease in molecular level is a newer practice with respect to the detection of complete remission by conventional pathologic analysis. Prognostic value of MRD in pediatric ALL (p-ALL) is well known. Objectives This study was aimed to describe clinical outcomes and prognosis, that is, overall survival and relapse in the patients with pBALL with respect to minimal residual disease detection on day 15, day 29, and postconsolidations in a tertiary care center in eastern India. Materials and Methods Eight color flow cytometry was used to detect MRD in this study. This contained markers such as CD 19, CD 34, CD 10, CD58, CD 45, CD13, anti-TDT, CD33. Eight panels included were (1) CMPO-FITC/cCD79a-PE/cCd3ECD, (2) CD20-FITC/cCD10-PE/cCd-19ECD, (3) CD34-FITC/cCD117-PE/cCd45 ECD/CD2 PC 5, (4) CD15 FITC/CD33PE/CD45ECD, (5) CD14 FITC/CD13 PE/CD45ECD, (6) HLADR FITC/CD7 PE/CD45 ECD, (7) TdT FITC/CD45 ECD (IF CD34 NEG), and (8) CD58 FITC/CD 45 ECD (IF BOTH CD34 AND TdT NEG; were used to prepare the marker. Results The study included 52 patients. In the 52 patients, 59.6% patients are alive with a p-value of 0.031. MRD was checked on every 15th and the 29th day and postconsolidation of the treatment where in day 15 (p = 0.023), it was 53.4% positive and 46.5% negative. On day 29 (p = 0.031), MRD was 22.5% positive and 77.5% negative, in post consolidation, it was positive in 20% and negative is 80%. MRD value below 0.01 is taken as negative and above is taken as positive. The overall survival (OS) is of 32.88 + 8.59 with a 6 to 36 months of duration. In In relapsed cases, no hemorrhagic relapse was found and two CNS relapse were found. Conclusion It was a study of 52 patients of pBALL with a detection of MRD by FCM. MRD-negative patients had a good prognosis and comparatively lower rate of relapse than the one with positive MRD. Effort should be made to adhere to recommendation of MRD testing in clinical guidelines.

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Azevedo, Isaclaudia G. D., Adriana Vieira-de-Abreu, André C. Ferreira, Danielle O. Nascimento, Hugo C. Castro-Faria-Neto, and Guy Zimmerman. "Integrin ADb2 (CD11d/CD18) Mediates Acute Lung Injury In Experimental Malaria." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1342.

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Khanna, Swati, Francis Mussai, Anish Thomas, Gary Middleton, Constance Yuan, Betsy Morrow, Jingli Zhang, Ira Pastan, Maryalice Stetler-Stevenson, and Raffit Hassan. "Abstract 3247: Granulocytic MDSCs (CD11b+CD15+CD14-HLADR-) in peripheral blood of mesothelioma patients are elevated and suppress T cell proliferation and function via reactive oxygen species." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3247.

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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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Cairns, AP, AD Crockard, and AL Bell. "THU0084 The cd14+/cd16+monocye subset in rheumatoid arthritis and systemic lupus erythematosus." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.961.

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Kim, J., S. J. Yoo, Y. Kim, S. W. Kang, S. C. Shim, and S. M. Kim. "SAT0064 Cd14+cd16+ monocyte subpopulation is dominant in the inflammation of osteoarthritis synovial fluid." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5140.

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Osterholzer, John J., Gwo-Hsiao Chen, Michal A. Olszewski, Jeffrey L. Curtis, and Galen B. Toews. "Classically-activated CD11c+ CD11b+ Exudate Macrophages Are Derived From Recruited Ly6C-high CD11b+ Monocytes In The Lungs Of Mice With Fungal Pneumonia." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5118.

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Ruzsics, István, Margit Tőkés-Füzesi, Marianna Matancic, Veronika Sárosi, Gábor Woth, and Tihamér Molnár. "Predictive value of CD14 and CD31 microparticles for the survival of COPD during 7 years." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa3852.

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Freeman, C. M., J. P. Brown, M. R. Kady, V. R. Stolberg, M. S. Toma, N. E. Alexis, M. Arjomandi, et al. "Intermediate (CD14++ CD16+) Monocytes Correlate with Parametric Response Mapping of Functional Small Airways Disease: Spiromics Immunophenotyping Sub-Study." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1063.

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Flavell, David J., Suzanne E. Holmes, Emily L. Gibbs, Jennifer E. Adcott, Sopsamorn U. Flavell, Christopher Bachran, Hendrik Fuchs, Alexander Weng, Diana Bachran, and Matthias F. Melzig. "Abstract 767:Gypsophilasaponins significantly augment the cytotoxicity of saporin-based anti-CD19, -CD22, -CD38 and -CD71 immunotoxins in human leukemia and lymphoma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-767.

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Reports on the topic "CD11"

Yang, Xiuwei. Critical Roles of CD151-alpha6beta1 and CD151-alpha6beta4 Integrin Complexes in Human Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada517279.

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Brutkiewicz, Randy. Regulation of CD1d-Medicated Antigen Presentation by Nf1. Fort Belvoir, VA: Defense Technical Information Center, February 2012. http://dx.doi.org/10.21236/ada560605.

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Yang, Xiuwei. CD151 Synergy With ErbB Receptors During Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada501759.

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Smith, Kyle, Julio Marsella, R. Kershaw, K. Dwight, and A. Wold. Preparation and Characterization of Cd1-xFexSe Single Crystals. Fort Belvoir, VA: Defense Technical Information Center, July 1988. http://dx.doi.org/10.21236/ada197890.

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Chen, Xiuxu, and Jenny E. Gumperz. Human CD1d-Restricted Natural Killer T (NKT) Cell Cytotoxicity Against Myeloid Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada462826.

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Hemler, Martin E. Targeting of CD151 in Breast Cancer and in Breast Cancer Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada477433.

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Terai, Kenta. How Alterations in the Cdt1 Expression Leads to Gene Amplification in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada514046.

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Terai, Kenta. How Alterations in the Cdt1 Expression Lead to Gene Amplification in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada549648.

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Kancheva, Lyudmila, Petar Nikolov, Tsvetelina Velikova, Ivan Valkov, Rossen Nikolov, and Lyudmila Mateva. Soluble CD14 is Associated with Disease Activity and Severity in Chronic Viral Hepatitis C and B. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, June 2018. http://dx.doi.org/10.7546/crabs.2018.06.17.

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Althoff, J. L., M. L. Apicella, and S. Singh. Integrated Information Support System (IISS). Volume 5. Common Data Model Subsystem. Part 3. CDM1: IDEF1 Model of the CDM -- CDM Development Specification. Fort Belvoir, VA: Defense Technical Information Center, September 1990. http://dx.doi.org/10.21236/ada252448.

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Academic literature on the topic 'CD11'

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Journal articles on the topic "CD11"

Dissertations / Theses on the topic "CD11"

Books on the topic "CD11"

Book chapters on the topic "CD11"

Conference papers on the topic "CD11"

Reports on the topic "CD11"