scholarly journals The influence of paediatric HIV infection on circulating B cell subsets and CXCR5 + T helper cells

2015 ◽  
Vol 181 (1) ◽  
pp. 110-117 ◽  
Author(s):  
A. Bamford ◽  
M. Hart ◽  
H. Lyall ◽  
D. Goldblatt ◽  
P. Kelleher ◽  
...  
Keyword(s):  
Hiv Infection ◽  
B Cell ◽  
T Helper Cells ◽  
T Helper ◽  
Paediatric Hiv ◽  
Helper Cells ◽  
B Cell Subsets ◽  
Paediatric Hiv Infection

scholarly journals Aberrant alteration of follicular T helper cells in ulcerative colitis patients and its correlations with interleukin-21 and B cell subsets

Medicine ◽  
2019 ◽  
Vol 98 (10) ◽  
pp. e14757 ◽  
Author(s):  
Guohui Xue ◽  
Yao Zhong ◽  
Lin Hua ◽  
Meijun Zhong ◽  
Xiaofeng Liu ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
B Cell ◽  
T Helper Cells ◽  
T Helper ◽  
Helper Cells ◽  
Interleukin 21 ◽  
B Cell Subsets ◽  
Follicular T Helper Cells

Functional and Chemical Characterization of B-Cell Growth Factor Produced by Normal Cloned T Helper Cells

1984 ◽  
Vol 20 (1) ◽  
pp. 7-14 ◽  
Author(s):  
S. PETTERSSON ◽  
T. LEANDERSSON ◽  
S. FORSGREN ◽  
G. POBOR ◽  
A. COUTINHO
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
B Cell ◽  
T Helper Cells ◽  
Chemical Characterization ◽  
T Helper ◽  
Helper Cells ◽  
B Cell Growth Factor

scholarly journals Role of accessory cells in cytokine production by T cells in chronic B- cell lymphocytic leukemia

Blood ◽  
1995 ◽  
Vol 86 (3) ◽  
pp. 1115-1123 ◽  
Author(s):  
T Decker ◽  
T Flohr ◽  
P Trautmann ◽  
MJ Aman ◽  
W Holter ◽  
...  
Keyword(s):  
T Cells ◽  
B Cell ◽  
T Helper Cells ◽  
Cytokine Production ◽  
Lymphocytic Leukemia ◽  
T Helper ◽  
Ifn Gamma ◽  
Helper Cells ◽  
Accessory Cells ◽  
Normal Individuals

Abstract We investigated the production of cytokines by highly purified T helper cells from B-cell chronic lymphocytic leukemia (B-CLL) patients stimulated by different activation pathways, and we studied the influence of various accessory cell populations on the pattern of the secretion of cytokines, including interleukin (IL)-2, IL-4, interferon- gamma (IFN-gamma), and IL-10. Neither a qualitative nor a quantitative difference in cytokine production and proliferative capacity was observed in CLL-derived purified T cells compared with normal individuals, when T cells were stimulated by different pathways, including CD3, CD2, and costimulation with CD28. Addition of autologous accessory cells (aAC), however, dramatically influenced the cytokine pattern of normal versus B-CLL-derived T cells. CLL cells as aAC caused a marked increase of IL-2, whereas IFN-gamma was only slightly induced and IL-4 was not influenced. In contrast, in normal individuals addition of aAC, which predominantly consisted of monocytes, resulted in a significant increase of IFN-gamma and a reduction of IL-4 secretion. IL-2 production was inhibited by higher concentrations of aAC. The increased stimulation of IL-2 production by CLL cells was not specific to the leukemic cell population, as purified B cells from normal individuals had the same effect. On the other hand, purified monocytes from CLL patients and controls both induced IFN-gamma production and inhibited IL-4 secretion. After antigen-specific stimulation with tetanus toxoid, cytokine secretion was influenced by the type of aAC in a similar pattern. We conclude that T helper cells derived from patients with B-CLL are intrinsically normal and that the predominance of B cells as accessory cells in CLL significantly alters the immune function of T helper cells in vitro.

scholarly journals Dual regulation of IRF4 function in T and B cells is required for the coordination of T–B cell interactions and the prevention of autoimmunity

2012 ◽  
Vol 209 (3) ◽  
pp. 581-596 ◽  
Author(s):  
Partha S. Biswas ◽  
Sanjay Gupta ◽  
Roslynn A. Stirzaker ◽  
Varsha Kumar ◽  
Rolf Jessberger ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
B Cells ◽  
B Cell ◽  
Lupus Erythematosus ◽  
T Helper Cells ◽  
Regulatory Protein ◽  
Cell Interactions ◽  
T Helper ◽  
T And B Cells ◽  
Helper Cells

Effective humoral responses to protein antigens require the precise execution of carefully timed differentiation programs in both T and B cell compartments. Disturbances in this process underlie the pathogenesis of many autoimmune disorders, including systemic lupus erythematosus (SLE). Interferon regulatory factor 4 (IRF4) is induced upon the activation of T and B cells and serves critical functions. In CD4+ T helper cells, IRF4 plays an essential role in the regulation of IL-21 production, whereas in B cells it controls class switch recombination and plasma cell differentiation. IRF4 function in T helper cells can be modulated by its interaction with regulatory protein DEF6, a molecule that shares a high degree of homology with only one other protein, SWAP-70. Here, we demonstrate that on a C57BL/6 background the absence of both DEF6 and SWAP-70 leads to the development of a lupus-like disease in female mice, marked by simultaneous deregulation of CD4+ T cell IL-21 production and increased IL-21 B cell responsiveness. We furthermore show that DEF6 and SWAP-70 are differentially used at distinct stages of B cell differentiation to selectively control the ability of IRF4 to regulate IL-21 responsiveness in a stage-specific manner. Collectively, these data provide novel insights into the mechanisms that normally couple and coordinately regulate T and B cell responses to ensure tight control of productive T–B cell interactions.

scholarly journals A Rapid-Response Humoral Vaccine Platform Exploiting Pre-Existing Non-Cognate Populations of Anti-Vaccine or Anti-Viral CD4+ T Helper Cells to Confirm B Cell Activation

PLoS ONE ◽  
2016 ◽  
Vol 11 (11) ◽  
pp. e0166383 ◽  
Author(s):  
Thomas Hills ◽  
Phillip G. Jakeman ◽  
Robert C. Carlisle ◽  
Paul Klenerman ◽  
Leonard W. Seymour ◽  
...  
Keyword(s):  
B Cell ◽  
T Helper Cells ◽  
Cell Activation ◽  
Rapid Response ◽  
B Cell Activation ◽  
T Helper ◽  
Vaccine Platform ◽  
Helper Cells

scholarly journals B Cell Depletion Reduces the Number of Autoreactive T Helper Cells and Prevents Glucose-6-Phosphate Isomerase-Induced Arthritis

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e24718 ◽  
Author(s):  
Oliver Frey ◽  
Lisa Bruns ◽  
Lars Morawietz ◽  
Kyri Dunussi-Joannopoulos ◽  
Thomas Kamradt
Keyword(s):  
B Cell ◽  
T Helper Cells ◽  
Cell Depletion ◽  
B Cell Depletion ◽  
T Helper ◽  
Helper Cells

scholarly journals Idiotype-recognizing T helper cells that are not idiotype specific.

1983 ◽  
Vol 158 (3) ◽  
pp. 811-821 ◽  
Author(s):  
M McNamara ◽  
H Kohler
Keyword(s):  
T Cells ◽  
B Cell ◽  
Cell Response ◽  
T Helper Cells ◽  
Helper Cell ◽  
T Helper ◽  
Helper Cells ◽  
Limiting Dilution ◽  
Selection Of ◽  
B Cell Response

In this study T helper cells that recognize idiotypes as carriers for a hapten-specific B cell response were analyzed under limiting dilution conditions. T helper cells, induced by phosphorylcholine-hemocyanin (PC-Hy) priming, recognize trinitrophenylated TEPC-15 and MOPC-167 (TNP-T15, TNP-167) equally well. Limiting dilution analysis indicates identical frequencies of helper cells for TNP-T15 and TNP-167. Double immunization protocols using TNP-T15 and TNP-167 fail to demonstrate additive effects. Inhibition of carrier recognition in vitro using free hapten, PC, and unconjugated T15 or M167 indicates identical specificities of helper cells for T15 and M167. Collectively, these results provide strong evidence that PC-Hy priming induces only one population of idiotype-recognizing helper cells that are unable to distinguish between the T15 and the M167 idiotopes. The helper cell induction circuit was further analyzed. PC-Hy priming induces T15/167-specific helper T cells in X-linked immune defect-expressing F1 mice. This indicates that a B cell response to PC is not required to induce idiotype-recognizing T cells. Adoptive cotransfer of B cells from PC-Hy-primed mice together with normal T cells fails to induce idiotype-recognizing T cells. These results indicate the existence of a T helper1-T helper2 induction loop. In this scheme, the T helper1 cell carries T15-like receptors and the T helper2 cells, anti-T15-like receptors. Monoclonal antiidiotypic antibodies specific for T15 also induce a T15/167-recognizing T helper cell population. This finding demonstrates that idiotope-specific priming induces non-idiotype-specific T cells. Evidently, the idiotypic T cell network is based on a different selection of idiotope determinants than the selection of the B cell idiotype network.

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