Transforming growth factor beta specifically enhances IgA production by lipopolysaccharide-stimulated murine B lymphocytes.

Coffman, Robert L.; Lebman, Deborah A.; Shrader, B

doi:10.1084/jem.170.3.1039

Cited by 531 publications

(251 citation statements)

References 18 publications

(8 reference statements)

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“…In conclusion, TGF-β1 is a well known cytokine that induce isotype switching recombination of IgA in mouse B cells (Coffman et al, 1989;Kim and Kagnoff, 1990). It is generally accepted that activated Th cells produce these cytokines which in turn directly modulate B cells.…”

Section: Discussionmentioning

confidence: 97%

TGF-β1 Stimulates Mouse Macrophages to Express APRIL through Smad and p38MAPK/CREB Pathways

Jang¹,

Kim²,

Seo³

et al. 2011

Molecules and Cells

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Section: Discussionmentioning

confidence: 97%

TGF-β1 Stimulates Mouse Macrophages to Express APRIL through Smad and p38MAPK/CREB Pathways

Jang¹,

Kim²,

Seo³

et al. 2011

Molecules and Cells

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“…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%

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 the present experiment, IgA anti-OvA levels were suppressed in the OvA-fed rats. An increased TGF-b production could be expected to lead to a deviation of the immune response towards an increase in IgA levels, as TGF-b is a switch factor for IgA [24]. However, the activation of a regulatory T cell population with no IL-4 secretion apparently led to decreased B cell help, resulting in suppressed levels of all isotypes of antibodies.…”

Section: Discussionmentioning

confidence: 99%

Active suppression in orally tolerized rats coincides within situtransforming growth factor-beta (TGF-β) expression in the draining lymph nodes

Lundin

Karlsson

Svensson

et al. 1999

Clinical and Experimental Immunology

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SUMMARYAdult rats were fed pellets containing ovalbumin (OvA) during 4 weeks, and were 2 weeks thereafter immunized subcutaneously with a mixture of OvA and human serum albumin (HSA) in Freund's complete adjuvant (day 0). As a result of the immunization, the draining lymph nodes of the nontolerized (control) rats were heavily enlarged from day 10 to day 18; however, this size increase was absent in the OvA-fed rats. This manifestation of active suppression in the tolerized rats was preceded by the appearance of scattered CD4 þ TGF-b-expressing T cells in the T cell area of their lymph nodes (days 5-8); correspondingly, the levels of TGF-b mRNA in the nodes were elevated in the tolerant rats compared with the control rats. The anti-OvA antibody levels in sera from the rats revealed that there was an initial B cell priming in the OvA-fed group, with levels higher than in the control group during the first week. Thereafter, suppression governed the response, and from day 10 onwards the anti-OvA levels were considerably lower than in the controls. When other groups of animals were pretreated with neutralizing anti-TGF-b antibodies 1 day before the immunization, the anti-OvA response of the OvAfed rats was restored to the levels of the control group, demonstrating the importance of TGF-b in the maintenance of suppression.In conclusion, we demonstrate that TGF-b-producing cells appear in the draining lymph nodes shortly after immunization in rats made orally tolerant using a relatively highdose feeding regime; these cells are probably responsible for the down-regulation of the immune response observed in the OvA-fed rats.

show abstract

Transforming growth factor beta specifically enhances IgA production by lipopolysaccharide-stimulated murine B lymphocytes.

Cited by 531 publications

References 18 publications

TGF-β1 Stimulates Mouse Macrophages to Express APRIL through Smad and p38MAPK/CREB Pathways

TGF-β1 Stimulates Mouse Macrophages to Express APRIL through Smad and p38MAPK/CREB Pathways

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

Active suppression in orally tolerized rats coincides within situtransforming growth factor-beta (TGF-β) expression in the draining lymph nodes

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