IL-10 selectively regulates murine Ig isotype switching

Shparago, Neil; Żelazowski, Piotr; Jin, Liang; Mclntyre, Tina M.; Stüber, Eckhard; Pecanha, L. M. T.; Kehry, Marilyn R.; Mond, James J.; Max, Edward E.; Snapper, Clifford M.

doi:10.1093/intimm/8.5.781

Cited by 43 publications

(35 citation statements)

References 36 publications

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“…IgM and IgG3 are the predominant isotypes secreted by marginal zone B cells, and these are the isotypes of the neutralizing Abs that are detected early after infection of mice with FMDV (7). The secretion of IFN-␥ and IL-10 by splenocytes stimulated by FMDV-infected DCs is also consistent with the production of IgG3 during this early stage, because these cytokines promote a switch toward this isotype (47,48). These TI-neutralizing Abs are sufficient to clear the virus in 3 days after infection.…”

Section: Discussionsupporting

confidence: 68%

Impairment of Thymus-Dependent Responses by Murine Dendritic Cells Infected with Foot-and-Mouth Disease Virus

Ostrowski

Vermeulen

Zábal

et al. 2005

The Journal of Immunology

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Foot-and-mouth disease virus (FMDV) is a cytopathic virus that experimentally infects mice, inducing a thymus-independent neutralizing Ab response that rapidly clears the virus. In contrast, vaccination with UV-inactivated virus induces a typical thymus-dependent (TD) response. In this study we show that dendritic cells (DCs) are susceptible to infection with FMDV in vitro, although viral replication is abortive. Infected DCs down-regulate the expression of MHC class II and CD40 molecules and up-regulate the expression of CD11b. In addition, infected DCs exhibit morphological and functional changes toward a macrophage-like phenotype. FMDV-infected DCs fail to stimulate T cell proliferation in vitro and to boost an Ab response in vivo. Moreover, infection of DCs in vitro induces the secretion of IFN-γ and the suppressive cytokine IL-10 in cocultures of DCs and splenocytes. High quantities of these cytokines are also detected in the spleens of FMDV-infected mice, but not in the spleens of vaccinated mice. The peak secretion of IFN-γ and IL-10 is concurrent with the suppression of Con A-mediated proliferation of T cells obtained from the spleens of infected mice. Furthermore, the secretion of these cytokines correlates with the suppression of the response to OVA, a typical TD Ag. Thus, infection of DCs with FMDV induces suppression of TD responses without affecting the induction of a protective thymus-independent response. Later, T cell responses are restored, setting the stage for the development of a long-lasting protective immunity.

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Section: Discussionsupporting

confidence: 68%

Impairment of Thymus-Dependent Responses by Murine Dendritic Cells Infected with Foot-and-Mouth Disease Virus

Ostrowski

Vermeulen

Zábal

et al. 2005

The Journal of Immunology

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“…IL-10 may also act later during the adaptive phase of the humoral response to R36A by inhibiting CD28 signaling, through a direct effect on T cells (38). Further, IL-10 can act directly on B cells to stimulate switching to IgG3 (70), but this effect was not observed in response to R36A.…”

Section: Discussionmentioning

confidence: 99%

Endogenous Pro- and Anti-Inflammatory Cytokines Differentially Regulate an In Vivo Humoral Response toStreptococcus pneumoniae

Khan

Shen

et al. 2002

Infect Immun

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؊/؊ mice. In this regard, a marked enhancement in the induction of proinflammatory cytokines was observed in the absence of IL-10, relative to controls. Ig isotype titers specific for the phosphorycholine determinant of C-polysaccharide were similarly regulated, but to a much more modest degree. These data suggest that proinflammatory and anti-inflammatory cytokines differentially regulate an in vivo protein-and polysaccharide-specific Ig response to an extracellular bacteria.

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“…The dramatic increase in IgG3 levels seen in B6 mice (and to a much lesser extent in CD4 KO mice) may be regulated by IL-10 production. This cytokine has been shown to promote switching to IgG3 in LPS-activated B cells (35) and is produced in elevated amounts by splenic cells from MAIDS-infected mice (36). These results show that the absence of CD4 on T cells has the effect of down-regulating in vivo Ab responses during MAIDS infection, and furthermore that the interaction of CD4 with class II, on the B cells, provides signals required for isotype switching and terminal differentiation.…”

Section: Ref 23)mentioning

confidence: 99%

B Cell Immunodeficiency Fails to Develop in CD4-Deficient Mice Infected with BM5: Murine AIDS as a Multistep Disease

Harris

Koch

Mullen

et al. 2001

The Journal of Immunology

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The immunodeficiency syndrome murine AIDS (MAIDS), caused by the BM5 retrovirus preparation, involves the activation, division, and subsequent anergy of the entire CD4+ T cell population as well as extensive B cell hyperproliferation and hypergammaglobulinemia, resulting in splenomegaly and lymphadenopathy, followed many weeks later by death. The development of MAIDS requires CD4+ T cells and MHC class II expression by the infected host, supporting a role for T-B interaction in disease development or progression. To explore this possibility, we examined development of MAIDS in mice deficient in CD4 (CD4 knockout), in which T-B interactions are compromised. We find that in CD4 knockout hosts, BM5 causes T cell immunodeficiency in the remaining T cells but has only a limited ability to induce B cell phenotypic changes, hyperproliferation, hypergammaglobulinemia, or splenomegaly. There is also delayed death of infected mice. This implies that CD4 dependent T-B interaction is needed to induce the B cell aspects of disease and supports a multistep mechanism of disease in which B cell changes follow and are caused by CD4+ T cell effects.

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IL-10 selectively regulates murine Ig isotype switching

Cited by 43 publications

References 36 publications

Impairment of Thymus-Dependent Responses by Murine Dendritic Cells Infected with Foot-and-Mouth Disease Virus

Impairment of Thymus-Dependent Responses by Murine Dendritic Cells Infected with Foot-and-Mouth Disease Virus

Endogenous Pro- and Anti-Inflammatory Cytokines Differentially Regulate an In Vivo Humoral Response toStreptococcus pneumoniae

B Cell Immunodeficiency Fails to Develop in CD4-Deficient Mice Infected with BM5: Murine AIDS as a Multistep Disease

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