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 Ability of antigen-specific helper cells to effect a class-restricted increase in total Ig-secreting cells in spleens after immunization with the antigen.

1979 ◽  
Vol 150 (3) ◽  
pp. 517-530 ◽  
Author(s):  
Y J Rosenberg ◽  
J M Chiller
Keyword(s):  
B Cells ◽  
B Lymphocytes ◽  
T Helper Cells ◽  
Cell Activation ◽  
Present Report ◽  
B Cell Activation ◽  
T Helper ◽  
Helper Cells ◽  
Large Numbers ◽  
Stimulation Of

Immunization with antigens stimulates not only B lymphocytes secreting specific antibody but, in addition, results in the generation of very large numbers of splenic Ig-secreting cells which lack specificity for that antigen. The present report examined the nature of the antigens capable of eliciting this effect and the mechanisms whereby B cells could be nonspecifically activated. It is shown that the ability of T-dependent, but not T-independent antigens, to induce such increases requires the participation of T helper cells specific for the antigen so that any one antigen results in the activation of only a proportion of total B cells. Analysis of this nonspecific plaque-forming-cell response reveals that B cell activation is not random but occurs in a class-restricted manner. The magnitude of the increase and the isotype produced are shown to be characteristic of the immunizing antigen. Based on the data presented, the apparent nonspecific T-B collaboration can best be explained by invoking a second Ig-specific helper mechanism in which helper cells capable of recognizing determinants on Ig molecules, e.g. isotype or idiotype, cause the stimulation of B cells of any specificity providing they express that determinant.

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 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 Dendritic Cell-Independent B Cell Activation During Acute Virus Infection: A Role for Early CCR7-Driven B-T Helper Cell Collaboration

2007 ◽  
Vol 178 (3) ◽  
pp. 1468-1476 ◽  
Author(s):  
Elke Scandella ◽  
Katja Fink ◽  
Tobias Junt ◽  
Beatrice M. Senn ◽  
Evelyn Lattmann ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Virus Infection ◽  
B Cell ◽  
Cell Activation ◽  
T Helper Cell ◽  
Helper Cell ◽  
B Cell Activation ◽  
T Helper

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 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
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