CD8(+)CD28(-) Regulatory T Lymphocytes Prevent Experimental Inflammatory Bowel Disease in Mice.
Background & Aims: Immune responses to innocuous intestinal antigens appear tightly controlled by regulatory T lymphocytes. While CD4(+) T lymphocytes have recently attracted the most attention, CD8(+) regulatory T-cell populations are also believed to play an important role in control of mucosal immunity. However, CD8(+) regulatory T-cell function has mainly been studied in vitro and no direct in vivo evidence exists that they can control mucosal immune responses. We investigated the capacity of CD8(+)CD28(-) T cells to prevent experimental inflammatory bowel disease (IBD) in mice. Methods: CD8(+)CD28(-) regulatory T cells were isolated from unmanipulated mice and tested for their capacity to inhibit T-cell activation in allogeneic mixed lymphocyte cultures in vitro and to prevent IBD induced by injection of CD4(+)CD45RB(high) cells into syngeneic immunodeficient RAG-2 mutant mice. Results: CD8(+)CD28(-) T lymphocytes inhibited proliferation and interferon gamma production by CD4(+) responder T cells in vitro. CD8(+)CD28(-) regulatory T cells freshly isolated from spleen or gut efficiently prevented IBD induced by transfer of colitogenic T cells into immunodeficient hosts. Regulatory CD8(+)CD28(-) T cells incapable of producing interleukin-10 did not prevent colitis. Moreover, IBD induced with colitogenic T cells incapable of responding to transforming growth factor beta could not be prevented with CD8(+)CD28(-) regulatory T cells. CD8(+)CD28(+) T cells did not inhibit in vitro or in vivo immune responses. Conclusions: Our findings show that naturally occurring CD8(+)CD28(-) regulatory T lymphocytes can prevent experimental IBD in mice and suggest that these cells may play an important role in control of mucosal immunity.[1]References
- CD8(+)CD28(-) Regulatory T Lymphocytes Prevent Experimental Inflammatory Bowel Disease in Mice. M??nager-Marcq, I., Pomi??, C., Romagnoli, P., van Meerwijk, J.P. Gastroenterology (2006) [Pubmed]
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