Human interleukin 10 induces naive surface immunoglobulin D+ (sIgD+) B cells to secrete IgG1 and IgG3.

Brière, Francine; Servet-Delprat, Christine; Bridon, Jean-Michel; Saint-Remy, Jean-Marie; Banchereau, Jacques

doi:10.1084/jem.179.2.757

Cited by 302 publications

(183 citation statements)

References 23 publications

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“…This is consistent with the fact that IL-10 acts mainly as a switching factor from IgM to IgG (37). Thus, IL-10 might play a crucial role in the antigen-driven production of autoreactive IgG by B cells after interaction with T helper cells in RA patients.…”

Section: Discussionsupporting

confidence: 87%

Association of the –2849 interleukin‐10 promoter polymorphism with autoantibody production and joint destruction in rheumatoid arthritis

Lard¹,

Gaalen²,

Schonkeren³

et al. 2003

Arthritis & Rheumatism

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Objective. To analyze the -2849 A/G interleukin-10 (IL-10) promoter polymorphism, which is associated with high (AG/GG) and low (AA) IL-10 production, in a cohort of rheumatoid arthritis (RA) patients and controls in order to gain a better understanding of its role in the incidence and progression of RA.Methods. Allele frequencies of the promoter polymorphism -2849 A/G and carriage rates were compared in 283 RA patients, 413 patients with other rheumatic diseases, and 1,220 healthy controls. The rate of joint damage and baseline levels of IgG and IgM rheumatoid factors and anti-citrullinated peptide antibodies were measured and were correlated with the IL-10 gene polymorphism. Furthermore, the correlation between the invasiveness of fibroblast-like synoviocytes (FLS) and the ؊2849 IL-10 genotype was tested.

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Section: Discussionsupporting

confidence: 87%

Association of the –2849 interleukin‐10 promoter polymorphism with autoantibody production and joint destruction in rheumatoid arthritis

Lard¹,

Gaalen²,

Schonkeren³

et al. 2003

Arthritis & Rheumatism

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“…However, in contrast to IL-4, IL-10 also promotes the Ig switch to IgG3 [68]. The effect of CD4 + KJ1-26 + cells from tolerant mice on promoting IgG1 but not IgG3 suggests a Th2-type cell rather than a Tr1-type regulatory cell.…”

Section: Discussionmentioning

confidence: 94%

“…The cytokine IL-10 also induces the switch to IgG1 [68]. However, in contrast to IL-4, IL-10 also promotes the Ig switch to IgG3 [68].…”

Section: Discussionmentioning

confidence: 99%

“…Thus, IL-4 promotes the isotype switch to IgG1 [62] and IgE [63,64], whereas IFN-γ promotes the isotype switch to IgG3 [65] and IgG2a [65,66]. TGF-β promotes the switch to IgA [67], and IL-10 promotes the switch to IgG1 and IgG3 [68]. Isotype switch indicates a maturation of the response and is associated with a decrease in secreted IgM, the isotype secreted early during the B cell response [69].…”

Section: Transgenic Mouse Model Systemmentioning

confidence: 99%

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CD8 blockade promotes the expansion of antigen-specific CD4+ FOXP3+ regulatory T cells in vivo

Wang

Davies

2007

International Immunopharmacology

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Treatment with a cocktail of CD4 and CD8-specific monoclonal antibodies (mAb) induces long-term transplantation tolerance and regulatory CD4 + T cells that induce tolerance in non-tolerant T cells. In contrast, treatment with a CD4-specific mAb alone fails to induce long-term tolerance. The current study was designed to test the hypothesis that CD8 blockade plays a role in promoting the development of CD4 + regulatory T cells.Using the DO11.10 CD4 + TCR transgenic mouse model we show that treatment with a CD4/CD8-specific mAb cocktail induces antigen-specific tolerance to OVA, measured by a significant decrease in OVA-specific IgG, on challenge with antigen. Although treatment with OVA and the CD4-specific mAb alone also induces a significant decrease in OVA-specific antibody, the number of DO11.10 cells is significantly greater in mice treated with the CD4/CD8-specific mAb cocktail, and this is associated with a significant increase in proliferation of DO11.10 cells in response to specific antigen. DO11.10 cells sorted from mice made tolerant to OVA with the CD4/CD8-specific mAb cocktail promote an OVA-specific IgG1 (Th2-type) response but not an OVA-specific IgG3 (Th1-type) response on transfer into new syngeneic recipients, suggesting their ability to regulate the type of antigen-specific immune response that ensues after priming with antigen. In addition, DO11.10 cells from tolerant mice express markers that are characteristic of CD4 + regulatory cells, including FOXP3, GITR and CTLA4, but not CD25. Taken as a whole, these data suggest that CD8 blockade promotes CD4 + FOXP3 + regulatory CD4 + T cells by promoting their proliferation in tolerant mice.

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“…In chronic chagasic patients, IgG1 and IgG2 form about 90% of the IgG produced (Watthanakulpanich et al 2008). It has been demonstrated that Th1 cytokines (IL-12, IFN-γ, TNF-α) are responsible for the production of IgG1 and IgG3 isotypes, while Th2 cytokines (IL-4 and IL-10) stimulate IgG2 production (Briere et al 1994, Kawano et al 1994). IgG1 mediates lysis binding to complement C1q protein and macrophage phagocytosis, while IgG2 mediates immunity by non-phagocytic effectors cells (Fanger et al 1991).…”

mentioning

confidence: 99%

Immunological imbalance between IFN-³ and IL-10 levels in the sera of patients with the cardiac form of Chagas disease

D'avila

Guedes

Castro

et al. 2009

Mem. Inst. Oswaldo Cruz

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Human interleukin 10 induces naive surface immunoglobulin D+ (sIgD+) B cells to secrete IgG1 and IgG3.

Cited by 302 publications

References 23 publications

Association of the –2849 interleukin‐10 promoter polymorphism with autoantibody production and joint destruction in rheumatoid arthritis

Association of the –2849 interleukin‐10 promoter polymorphism with autoantibody production and joint destruction in rheumatoid arthritis

CD8 blockade promotes the expansion of antigen-specific CD4+ FOXP3+ regulatory T cells in vivo

Immunological imbalance between IFN-³ and IL-10 levels in the sera of patients with the cardiac form of Chagas disease

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