A limited course of soluble CD83 delays acute cellular rejection of MHC-mismatched mouse skin allografts

Xu, Jun‐Fa; Huang, Baojun; Yin, Hui; Xiong, Ping; Feng, Wen; Xu, Yong; Fang, Min; Zheng, Fang; Wang, Cong Yi; Gong, Feili

doi:10.1111/j.1432-2277.2006.00426.x

Cited by 51 publications

(48 citation statements)

References 36 publications

(45 reference statements)

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“…Administration of sCD83 in a murine skin transplantation model delayed skin rejection, and the prolonged graft survival was associated with inhibited allo-reactive T cell proliferation (23). Additionally, it has been shown that sCD83 injections markedly ameliorated the clinical symptoms associated with EAE under prophylactic and therapeutic settings (21).…”

Section: Discussionmentioning

confidence: 99%

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CD83 Expression in CD4+ T Cells Modulates Inflammation and Autoimmunity

Reinwald

Wiethe²,

Westendorf

et al. 2008

The Journal of Immunology

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The transmembrane protein CD83 has been initially described as a maturation marker for dendritic cells. Moreover, there is increasing evidence that CD83 also regulates B cell function, thymic T cell maturation, and peripheral T cell activation. Herein, we show that CD83 expression confers immunosuppressive function to CD4+ T cells. CD83 mRNA is differentially expressed in naturally occurring CD4+CD25+ regulatory T cells, and upon activation these cells rapidly express large amounts of surface CD83. Transduction of naive CD4+CD25− T cells with CD83 encoding retroviruses induces a regulatory phenotype in vitro, which is accompanied by the induction of Foxp3. Functional analysis of CD83-transduced T cells in vivo demonstrates that these CD83+Foxp3+ T cells are able to interfere with the effector phase of severe contact hypersensitivity reaction of the skin. Moreover, adoptive transfer of these cells prevents the paralysis associated with experimental autoimmune encephalomyelitis, suppresses proinflammatory cytokines IFN-γ and IL-17, and increases antiinflammatory IL-10 in recipient mice. Taken together, our data provide the first evidence that CD83 expression can contribute to the immunosuppressive function of CD4+ T cells in vivo.

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Section: Discussionmentioning

confidence: 99%

“…Additionally, they demonstrated that sCD83 down-modulates antitumor immune responses in vivo using the murine P815 tumor model (22). Most recently, Xu and colleagues have shown that a limited course of sCD83 delayed acute cellular rejection of MHC-mismatched mouse skin allografts (23).…”

mentioning

confidence: 99%

CD83 Expression in CD4+ T Cells Modulates Inflammation and Autoimmunity

Reinwald

Wiethe²,

Westendorf

et al. 2008

The Journal of Immunology

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“…The murine skin transplantation model is a broadly accepted model for the study of immunological mechanisms in allograft rejection that allows for easy surgical procedures, easy inspection, and repeatability (12). There is extensive evidence that the murine homolog of HLA-G is Qa-2 (13,14).…”

Section: And Xiong Zoumentioning

confidence: 99%

Differential Effects of HNF-1α Mutations Associated with Familial Young-Onset Diabetes on Target Gene Regulation

Galán

García-Herrero

Azriel

et al. 2010

Mol Med

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“…Several lines of evidence also suggest an implication of CD83 in the regulation of peripheral T cell responses (19). Addition of soluble CD83 species has been shown to inhibit murine T cell activation in vitro (20 -23) and to act immunosuppressive in vivo (24,25). Other groups, however, did not observe such suppressive effects in comparable systems (26).…”

mentioning

confidence: 99%

Engagement of CD83 on B Cells Modulates B Cell Function In Vivo

Kretschmer

Lüthje

Schneider

et al. 2009

The Journal of Immunology

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The transmembrane glycoprotein CD83 is an important regulator of both thymic T cell maturation and peripheral T cell response. Recent studies suggested that CD83 is also involved in the regulation of B cell maturation, activation, and homeostasis. In this study, we show that in vivo overexpression of CD83 dose dependently interfered with the Ig response to thymus-dependent and thymus-independent model Ag immunization. CD83 deficiency, in contrast, which was restricted to B cells in mixed bone marrow chimeras, led to unchanged or even slightly increased Ig responses. Strikingly, the engagement of CD83 that is naturally upregulated on wild-type B cells by injection of anti-CD83 mAb in vivo induced a 100-fold increase in the IgG1 response to immunization. Kinetic analysis revealed that CD83 had to be engaged simultaneously or shortly after the B cell activation through injection of Ag, to modulate the IgG1 secretion. Furthermore, using mixed bone marrow chimeras in which either selectively the B cells or the dendritic cells were CD83 deficient, we demonstrate that anti-CD83 mAb mediated its biologic effect by engaging CD83 on B cells and not on CD11c ؉ dendritic cells. Taken together, we provide strong evidence that CD83 transduces regulatory signals into the very B cell on which it is expressed.

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A limited course of soluble CD83 delays acute cellular rejection of MHC-mismatched mouse skin allografts

Cited by 51 publications

References 36 publications

CD83 Expression in CD4+ T Cells Modulates Inflammation and Autoimmunity

CD83 Expression in CD4+ T Cells Modulates Inflammation and Autoimmunity

Differential Effects of HNF-1α Mutations Associated with Familial Young-Onset Diabetes on Target Gene Regulation

Engagement of CD83 on B Cells Modulates B Cell Function In Vivo

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