B1 Cells Contribute to Serum IgM, But Not to Intestinal IgA, Production in Gnotobiotic Ig Allotype Chimeric Mice

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.

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Conjugated linoleic acid feeding during rat suckling period enhances intestinal IgA production

Proceedings of The Nutrition Society ◽

10.1017/s0029665108006265 ◽

2008 ◽

Vol 67 (OCE1) ◽

Author(s):

F. J. Pérez-Cano ◽

M. Molero ◽

C. Ramírez-Santana ◽

M. Castell ◽

C. Castellote ◽

...

Keyword(s):

Linoleic Acid ◽

Conjugated Linoleic Acid ◽

Suckling Period ◽

Iga Production ◽

Intestinal Iga

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Cocoa and cocoa fibre differentially modulate IgA and IgM production at mucosal sites

British Journal Of Nutrition ◽

10.1017/s000711451600074x ◽

2016 ◽

Vol 115 (9) ◽

pp. 1539-1546 ◽

Cited By ~ 11

Author(s):

Malen Massot-Cladera ◽

Àngels Franch ◽

Francisco J. Pérez-Cano ◽

Margarida Castell

Keyword(s):

Salivary Glands ◽

Standard Diet ◽

Mesenteric Lymph Nodes ◽

Gene Expressions ◽

Mesenteric Lymph ◽

Mucosal Tissues ◽

Serum Iga ◽

Iga Production ◽

The Impact ◽

Intestinal Iga

AbstractPrevious studies have shown that a 10 % cocoa (C10) diet, containing polyphenols and fibre among others, modifies intestinal and systemic Ig production. The present study aimed at evaluating the impact of C10 on IgA and IgM production in the intestinal and extra-intestinal mucosal compartments, establishing the involvement of cocoa fibre (CF) in such effects. Mechanisms by which C10 intake may affect IgA synthesis in the salivary glands were also studied. To this effect, rats were fed either a standard diet, a diet containing C10, CF or inulin. Intestinal (the gut wash (GW), Peyer’s patches (PP) and mesenteric lymph nodes (MLN)) and extra-intestinal (salivary glands) mucosal tissues and blood samples were collected for IgA and IgM quantification. The gene expressions of IgA production- and homing-related molecules were studied in the salivary glands. The C10 diet decreased intestinal IgA and IgM production. Although the CF diet decreased the GW IgA concentration, it increased PP, MLN and serum IgA concentrations. Both the C10 and the CF diets produced a down-regulatory effect on IgA secretion in the extra-intestinal tissues. The C10 diet interacted with the mechanisms involved in IgA synthesis, whereas the CF showed particular effects on the homing and transcytosis of IgA across the salivary glands. Overall, CF was able to up-regulate IgA production in the intestinal-inductor compartments, whereas it down-regulated its production at the mucosal-effector ones. Further studies must be directed to ascertain the mechanisms involved in the effect of particular cocoa components on gut-associated lymphoid tissue.

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Low Intestinal IGA Production in CVID Facilitates Pathobiont-Mediated IFN Responses and Enteropathy

Gastroenterology ◽

10.1016/s0016-5085(17)33381-4 ◽

2017 ◽

Vol 152 (5) ◽

pp. S997-S998 ◽

Cited By ~ 1

Author(s):

Natalia shulzhenko ◽

Xiaoxi Dong ◽

Dariia Vyshenska ◽

Renee Greer ◽

Manoj Gurung ◽

...

Keyword(s):

Iga Production ◽

Intestinal Iga

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IgM- and IgA-response of peritoneal B-1 cells to the TI-2 antigen with the presence of γδT cells in vitro

Medical Immunology (Russia) ◽

10.15789/1563-0625-iai-2157 ◽

2021 ◽

Vol 23 (2) ◽

pp. 245-256

Author(s):

N. A. Snegireva ◽

E. V. Sidorova ◽

I. N. Dyakov ◽

M. V. Gavrilova ◽

I. N. Chernyshova ◽

...

Keyword(s):

Mrna Expression ◽

Inflammatory Diseases ◽

The Body ◽

Γδt Cells ◽

Heavy Chains ◽

Iga Response ◽

Iga Production ◽

B1 Cells

IgA is an important component of the mucosal system of the body. It limits penetration of pathogens into the bloodstream. Inflammatory diseases such as Crohn disease and colitis may be associated with disorders of IgA synthesis. Both B1 and B2 cells are a source of IgA in the intestines. Special attention is paid to B1 cells, which are able to respond to T-independent type 2 antigens and produce natural antibodies. B1 cells produce about 50% of the intestinal IgA including specific antibodies to the components of microorganisms contained in the gastrointestinal tract. The mechanism of IgA formation in the T-independent way is not investigated in details. It was suggested that the γδТ-cells promote switching to IgA synthesis by B1 cells. This assumption may be supported by their co-localization with B1 lymphocytes in the intestinal mucosa, as well as participation, along with B1 cells, in formation of the first-line defense against the pathogens. In addition, the both lymphocyte subpopulations evolve during initial ontogenesis, earlier than “classic” В2 and αβT cells. Therefore, it was suggested that γδT lymphocytes may be involved into the processes of induction and/or regulation of IgM and IgA production by B1 cells in response to TH2 antigens.In the present study, we have shown the effect of γδT cells upon generation of IgM- and IgA-forming B1 cells in response to α-1,3-dextran in vitro. We also studied the dynamics of the mRNA expression for IgM- and IgA-heavy chains by the B1 cells at different terms of in vitro culture.It was found that, during co-cultivation of B1 cells with 20% γδT lymphocytes, there is no increase in the number of dextran-specific IgM-producing cells. The B1 cells exhibited an increase of IgM heavy chain mRNA expression in response to dextran but not in co-cultures. Expression of mRNA for IgM heavy chains in co-cultures was decreased compared to non-treated B-cell cultures. Contrary to the earlier assumption, a presence of γδT lymphocytes in culture did not enhance the formation of IgA producents. The obtained data suggest regulatory properties of the γδТ lymphocytes during the B1 cells response to T-independent antigens.

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Sphingosine 1‐phosphate regulates innate and acquired intestinal IgA production

The FASEB Journal ◽

10.1096/fasebj.22.1_supplement.853.17 ◽

2008 ◽

Vol 22 (S1) ◽

Author(s):

Jun Kunisawa ◽

Masashi Gohda ◽

Yosuke Kurashima ◽

Morio Higuchi ◽

Izumi Ishikawa ◽

...

Keyword(s):

Sphingosine 1 Phosphate ◽

Iga Production ◽

Intestinal Iga

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IgA dysfunctions induced by the early-lifetime disruption of gut microbitoa result in metabolic syndrome in mice

10.21203/rs.3.rs-40336/v1 ◽

2020 ◽

Author(s):

Jielong Guo ◽

Xue Han ◽

Yilin You ◽

Weidong Huang ◽

Zhan Jicheng

Keyword(s):

Metabolic Syndrome ◽

Low Dose ◽

Newborn Mice ◽

Germ Free ◽

Small Intestinal ◽

Iga Production ◽

Induced Changes ◽

Intestinal Iga

Abstract Backgroud: Disruption of the gut microbiota (GM), mainly induced by antibiotic treatments and C-sections, is prevalent during the early lifetime, which can result in lifelong changes in the GM composition and metabolism.Results: The GM of newborn mice was influenced after being subjected to transitory treatment with low-dose penicillin (LDP), resulting in a permanent reduction of intestinal IgA. Germ-free (GF) mice transferred GM from the LDP-treated mice also showed decreased intestinal IgA levels. Similarly, antigens derived from the LDP-treated mice induced lower IgA production during in vitro incubation with small intestinal tissues. Furthermore, a lack of intestinal IgA led to the persistent dysbiosis of mucosal GM, causing metabolic syndrome (MetS) in the LDP-treated mice. The mice lacking intestinal IgA (Pigr-/-) only showed transient alteration in GM after LDP exposure while the long-period metabolism was not influenced. Moreover, gavage with GM from the LDP-free mice or probiotics (partially) restored the GM and intestinal IgA, while improving the MetS in LDP-treated mice.Conclusions: The antibiotics–induced changes of GM in early lifetime permanently dampened the IgA responses to the GM, which lead to the long-term dysbiosis of intestinal mucosal bacteria and MetS.

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