scholarly journals New insights into immune mechanisms of antiperlecan/LG3 antibody production: Importance of T cells and innate B1 cells

2018 ◽  
Vol 19 (3) ◽  
pp. 699-712 ◽  
Author(s):  
Lauriane Padet ◽  
Mélanie Dieudé ◽  
Annie Karakeussian‐Rimbaud ◽  
Bing Yang ◽  
Julie Turgeon ◽  
...  
Keyword(s):  
T Cells ◽  
Antibody Production ◽  
Immune Mechanisms ◽  
B1 Cells

T cell-dependent suppression of antibody production. I. Characteristics of suppressor T cells following tolerance induction

1978 ◽  
Vol 8 (5) ◽  
pp. 360-370 ◽  
Author(s):  
A. Basten ◽  
J. F. A. P. Miller ◽  
R. Loblay ◽  
P. Johnson ◽  
Jennifer Gamble ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Antibody Production ◽  
Tolerance Induction ◽  
Suppressor T Cells ◽  
Suppression Of Antibody Production

scholarly journals B2 but Not B1 Cells Can Contribute to CD4+ T-Cell-Mediated Clearance of Rotavirus in SCID Mice

2001 ◽  
Vol 75 (12) ◽  
pp. 5482-5490 ◽  
Author(s):  
Natasha Kushnir ◽  
Nicolaas A. Bos ◽  
Adrian W. Zuercher ◽  
Susan E. Coffin ◽  
Charlotte A. Moser ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Secondary Infection ◽  
Immunoglobulin A ◽  
Cell Receptor ◽  
Scid Mice ◽  
Peritoneal Exudate ◽  
Peritoneal Exudate Cells ◽  
B1 Cells ◽  
Intestinal Iga

ABSTRACT Studies utilizing various immunodeficient mouse models of rotavirus (RV) infection demonstrated significant roles of RV-specific secretory immunoglobulin A (IgA), CD4+ T cells, and CD8+T cells in the clearance of RV and protection from secondary infection. Secretion of small but detectable amounts of IgA in RV-infected αβ T-cell receptor knockout mice (11) and distinctive anatomical localization and physiology of B1 cells suggested that B1 cells might be capable of producing RV-specific intestinal IgA in a T-cell-independent fashion and, therefore, be responsible for ablation of RV shedding. We investigated the role of B1 cells in the resolution of primary RV infection using a SCID mouse model. We found that the adoptive transfer of unseparated peritoneal exudate cells ablates RV shedding and leads to the production of high levels of RV-specific intestinal IgA. In contrast, purified B1 cells do not ablate RV shedding and do not induce a T-cell-independent or T-cell-dependent, RV-specific IgA response but do secrete large amounts of polyclonal (total) intestinal IgA. Cotransfer of mixtures of purified B1 cells and B1-cell-depleted peritoneal exudate cells differing in IgA allotypic markers also demonstrated that B2 cells (B1-cell-depleted peritoneal exudate cells) and not B1 cells produced RV-specific IgA. To our knowledge, this is the first observation that B1 cells are unable to cooperate with CD4+ T cells and produce virus-specific intestinal IgA antibody. We also observed that transferred CD4+ T cells alone are capable of resolving RV shedding, although no IgA is secreted. These data suggest that RV-specific IgA may not be obligatory for RV clearance but may protect from reinfection and that effector CD4+ T cells alone can mediate the resolution of primary RV infection. Reconstitution of RV-infected SCID mice with B1 cells results in the outgrowth of contaminating, donor CD4+ T cells that are unable to clear RV, possibly because their oligoclonal specificities may be ineffective against RV antigens.

Regulation of Immunoglobulin and Antibody Production Allotype Suppressor T Cells in Mice

1975 ◽  
Vol 27 (1) ◽  
pp. 57-83 ◽  
Author(s):  
Leonore A. Herzenberg ◽  
Ko Okumura ◽  
Charles M. Metzler
Keyword(s):  
T Cells ◽  
Antibody Production ◽  
Suppressor T Cells

scholarly journals GENETIC CONTROL OF THE IMMUNE RESPONSE

1972 ◽  
Vol 136 (5) ◽  
pp. 1195-1206 ◽  
Author(s):  
John C. Ordal ◽  
F. Carl Grumet
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Genetic Control ◽  
Antibody Production ◽  
Lymphoid Cells ◽  
Antigen Challenge ◽  
Graft Versus Host ◽  
K Cells

The transfer of parental (H-2k/k) nonresponder lymphoid cells into heterozygous (H-2k/q) nonresponder recipients at the time of primary challenge with aqueous poly-L(Tyr,Glu)-poly-D,L-Ala-poly-L-Lys [(T,G)-A--L] elicited the production of both IgM and IgG anti-(T,G)-A--L antibody. Normally, the production of IgG anti-(T,G)-A--L antibody is restricted to strains possessing the responder Ir-1 allele. The timing and intensity of the graft-versus-host (GVH) reaction required for this effect were found to be critical. Injection of H-2k/k cells into H-2k/q recipients 1 wk before antigen challenge did not elicit IgG anti-(T,G)-A--L antibody production, and markedly suppressed IgM anti-(T,G)-A--L antibody production. The transfer of alloimmune (H-2q-primed) H-2k/k cells at the time of antigen challenge was also associated with no IgG and little IgM anti-(T,G)-A--L antibody production. These data are consistent with the model that nonresponder thymus-derived lymphocytes (T cells) activated in a GVH reaction can substitute for (T,G)-A--L-reactive T cells to induce a shift from IgM to IgG anti-(T,G)-A--L antibody production.

Regulatory Immune Mechanisms beyond Regulatory T Cells

2019 ◽  
Vol 40 (6) ◽  
pp. 482-491 ◽  
Author(s):  
Gustaf Christoffersson ◽  
Matthias von Herrath
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Immune Mechanisms
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