Transfer Models of Colitis

Transfer of specific subsets ofT lymphocytes into immunocompromised (SCID) mice yields further information about the role of both IL-10 and T cell subsets in the regulation of the intestinal immune response. Transfer of the CD45RBhigh (naïve) subset of CD4+ cells into SCID mice induces colitis that does not occur with transfer of the CD45RBlow (memory) subset or coadministration of unfractionated CD4+ T cells.17 This suggests that there are regulatory factors within the CD45RBlow subset that are able to suppress the response of the CD45RB high subset to enteric antigens. The protective are independent of IL-4 suggesting that they are functionally distinct from Th2 cells. 8 IL-10

Transfer Model Colitis Scid Mice

Figure 3. The immunopathology of IL-10 -/- mice. In the absence of IL-10, the presentation of luminal antigen to mucosal T-cells leads to uninhibited IFN-y release that stimulates antigen presenting cell IL-12 release; this, in conjunction with the IFN-y leads to Th1 T cell differentiation. When presented with antigen, the Th1 cells drive macrophage pro-inflammatory cytokine release, which results in soluble mediator release and tissue damage.

Figure 3. The immunopathology of IL-10 -/- mice. In the absence of IL-10, the presentation of luminal antigen to mucosal T-cells leads to uninhibited IFN-y release that stimulates antigen presenting cell IL-12 release; this, in conjunction with the IFN-y leads to Th1 T cell differentiation. When presented with antigen, the Th1 cells drive macrophage pro-inflammatory cytokine release, which results in soluble mediator release and tissue damage.

therapy attenuates the colitis induced by CD45RBhigh CD4+ cells, conversely CD45RBlow CD4+ cells from an IL-10 -/- mouse are unable to prevent the colitis induced by CD45RB hlgh CD4+ cells.19 Indeed, both CD45RB low CD4+ and CD45RBhigh CD4+ subsets from IL-10 -/- mice induce colitis when transferred to RAG-2 -/- mice. These results cannot be attributed to developmental abnormalities in the IL-10 -/- mouse as blockade of IL-10 function using a monoclonal antibody against the IL-10 receptor abrogated the protective effect of CD45RBlow CD4+ cells from wild type mice.20 These results implicate IL-10 in the development and function of a subset of regulatory cells that protect against pathogenic responses to intestinal antigen.

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