scholarly journals Protective Immunity to Bordetella pertussis Requires Both B Cells and Cd4+ T Cells for Key Functions Other than Specific Antibody Production

2000 ◽  
Vol 191 (11) ◽  
pp. 1841-1852 ◽  
Author(s):  
Mary Leef ◽  
Karen L. Elkins ◽  
Jerko Barbic ◽  
Roberta D. Shahin
Keyword(s):  
T Cells ◽  
B Cells ◽  
Antibody Production ◽  
Bordetella Pertussis ◽  
Specific Antibody ◽  
Cd4 T Cells ◽  
Protective Immunity ◽  
Interleukin 10 ◽  
Interleukin 4 ◽  
Specific Antibody Production

To investigate the fundamental nature of protective immunity to Bordetella pertussis, we studied intranasal immunization of adult mice with formalin-fixed B. pertussis (FFBP), followed by aerosol B. pertussis challenge. Mice given two doses of FFBP intranasally completely cleared a subsequent pertussis aerosol challenge from tracheae and lungs (defined as protection), but there was no correlation between levels of specific antibody and clearance of bacteria. Further, transfer of immune serum before aerosol challenge had minimal effects on bacterial burdens. However, pertussis-specific T cells producing interferon γ but not interleukin 4 or interleukin 10 were detected in draining lymph nodes of FFBP-immunized mice. Significantly, repeated immunization of B cell knockout (BKO) mice resulted in partial protection, and complete protection was reconstituted by transfer of pertussis-immune B cells; reconstituted BKO mice had little if any detectable antipertussis antibodies. Immunization of mice lacking all T cells or lacking CD4+ T cells did not lead to protection; in contrast, CD8− mice were protected. Mice depleted of CD4+ T cells after immunization but before aerosol challenge, which thus had normal amounts of specific antibodies, were not optimally protected. Taken together, these data indicate that protective immunity to pertussis is dependent on both CD4+ T cells and B cells, and both cell types provide significant functions other than specific antibody production.

scholarly journals Viral Superantigen Drives Extrafollicular and Follicular B Cell Differentiation Leading to Virus-specific Antibody Production

1997 ◽  
Vol 185 (3) ◽  
pp. 551-562 ◽  
Author(s):  
Sanjiv A. Luther ◽  
Adam Gulbranson-Judge ◽  
Hans Acha-Orbea ◽  
Ian C.M. MacLennan
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
B Cells ◽  
B Cell ◽  
Antibody Production ◽  
Specific Antibody ◽  
Germinal Centers ◽  
B Cell Differentiation ◽  
Virus Specific Antibody ◽  
Specific Antibody Production

Mouse mammary tumor virus (MMTV[SW]) encodes a superantigen expressed by infected B cells. It evokes an antibody response specific for viral envelope protein, indicating selective activation of antigen-specific B cells. The response to MMTV(SW) in draining lymph nodes was compared with the response to haptenated chicken gamma globulin (NP-CGG) using flow cytometry and immunohistology. T cell priming occurs in both responses, with T cells proliferating in association with interdigitating dendritic cells in the T zone. T cell proliferation continues in the presence of B cells in the outer T zone, and B blasts then undergo exponential growth and differentiation into plasma cells in the medullary cords. Germinal centers develop in both responses, but those induced by MMTV(SW) appear later and are smaller. Most T cells activated in the T zone and germinal centers in the MMTV(SW) response are superantigen specific and these persist for weeks in lymph nodes draining the site MMTV(SW) injection; this contrasts with the selective loss of superantigen-specific T cells from other secondary lymphoid tissues. The results indicate that this viral superantigen, when expressed by professional antigen-presenting cells, drives extrafollicular and follicular B cell differentiation leading to virus-specific antibody production.

scholarly journals Intravenous tolerization with type II collagen induces interleukin‐4‐and interleukin‐10‐producing CD4 + T cells

Immunology ◽  
1999 ◽  
Vol 97 (3) ◽  
pp. 466-473 ◽  
Author(s):  
Gumanovskaya ◽  
Myers ◽  
Rosloniec ◽  
Stuart ◽  
Kang
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Type Ii Collagen ◽  
Interleukin 10 ◽  
Interleukin 4 ◽  
Type Ii

CD40 cross-linking inhibits specific antibody production by human B cells

1995 ◽  
Vol 7 (11) ◽  
pp. 1809-1815 ◽  
Author(s):  
Robin E. Callard ◽  
Joan Herbert ◽  
Susan H. Smith ◽  
Richard J. Armitage ◽  
Kathy E. Costelloe
Keyword(s):  
B Cells ◽  
Antibody Production ◽  
Specific Antibody ◽  
Cross Linking ◽  
Human B Cells ◽  
Specific Antibody Production

Ligation of B7 with CD28/CTLA-4 on T cells results in CD40 ligand expression, interleukin-4 secretion and efficient help for antibody production by B cells

1993 ◽  
Vol 23 (12) ◽  
pp. 3120-3125 ◽  
Author(s):  
Mark de Boer ◽  
Ahmad Kasran ◽  
Jaap Kwekkeboom ◽  
Hugo Walter ◽  
Peter Vandenberghe ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Antibody Production ◽  
Cd40 Ligand ◽  
Interleukin 4 ◽  
Ligand Expression

scholarly journals The presence of interleukin 4 during in vitro priming determines the lymphokine-producing potential of CD4+ T cells from T cell receptor transgenic mice.

1992 ◽  
Vol 176 (4) ◽  
pp. 1091-1098 ◽  
Author(s):  
R A Seder ◽  
W E Paul ◽  
M M Davis ◽  
B Fazekas de St Groth
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
T Cell Receptor ◽  
Cd4 T Cells ◽  
Cell Receptor ◽  
Inhibitory Effect ◽  
Interleukin 4 ◽  
Ifn Gamma

To study the factors that determine whether CD4+ T cells produce interleukin 4 (IL-4) or interferon gamma (IFN-gamma) upon stimulation we used a system allowing naive T cells to be primed in vitro by specific antigen. Dense CD4+ T cells were purified from mice that expressed transgenes encoding a T cell receptor specific for pigeon cytochrome C peptide 88-104 in association with I-Ek. These T cells produced very limited amounts of IL-4 and IFN-gamma upon immediate challenge with 88-104 and antigen-presenting cells (APC). However, after an initial "priming" culture in which they were incubated for 4 d in the presence of 88-104, APC, and 1,000 U/ml IL-4, the T cells acquired the capacity to produce substantial amounts of IL-4 upon rechallenge but made very little IFN-gamma. Cells primed in the absence of IL-4 produced IFN-gamma upon rechallenge but virtually no IL-4. The inhibitory effect of IL-4 on IFN-gamma production did not appear to be mediated by the induction of IL-10 production since IL-10 addition to initial cultures did not suppress priming for IFN-gamma production, nor did anti-IL-10 block the inhibitory effect of IL-4. IFN-gamma itself did not increase priming for IFN-gamma production, nor did anti-IFN-gamma reduce such priming. IFN-gamma did, however, diminish priming for IL-4 production when limiting amounts of IL-4 (100 U/ml) were used in the initial culture. The dominant effect of IL-4 in determining the lymphokine-producing phenotype of primed cells was observed with dendritic cells (DC), activated B cells, and I-Ek-transfected fibroblasts as APC. However, the different APC did vary in their potency, with DC being superior to activated B cells, which were superior to transfected fibroblasts.

scholarly journals The induction of antibody production by IL-6 is indirectly mediated by IL-21 produced by CD4+ T cells

2009 ◽  
Vol 206 (1) ◽  
pp. 69-78 ◽  
Author(s):  
Oliver Dienz ◽  
Sheri M. Eaton ◽  
Jeffrey P. Bond ◽  
Wendy Neveu ◽  
David Moquin ◽  
...  
Keyword(s):  
T Cells ◽  
B Cell ◽  
Antibody Production ◽  
Cd4 T Cells ◽  
Cell Receptor ◽  
Virus Specific Antibody ◽  
Specific Antibody Production ◽  
B Cell Growth Factor

Interleukin (IL) 6 is a proinflammtory cytokine produced by antigen-presenting cells and nonhematopoietic cells in response to external stimuli. It was initially identified as a B cell growth factor and inducer of plasma cell differentiation in vitro and plays an important role in antibody production and class switching in vivo. However, it is not clear whether IL-6 directly affects B cells or acts through other mechanisms. We show that IL-6 is sufficient and necessary to induce IL-21 production by naive and memory CD4+ T cells upon T cell receptor stimulation. IL-21 production by CD4+ T cells is required for IL-6 to promote B cell antibody production in vitro. Moreover, administration of IL-6 with inactive influenza virus enhances virus-specific antibody production, and importantly, this effect is dependent on IL-21. Thus, IL-6 promotes antibody production by promoting the B cell helper capabilities of CD4+ T cells through increased IL-21 production. IL-6 could therefore be a potential coadjuvant to enhance humoral immunity.

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