A role for NK cells as regulators of CD4+ T cells in a transfer model of colitis
| Autor: | M M, Fort, M W, Leach, D M, Rennick |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
CD4-Positive T-Lymphocytes
Mice Knockout Pore Forming Cytotoxic Proteins Membrane Glycoproteins Perforin Genes RAG-1 Graft Survival Colitis Lymphocyte Activation Adoptive Transfer Lymphocyte Depletion Interleukin-10 Killer Cells Natural Mice Inbred C57BL Disease Models Animal Mice T-Lymphocyte Subsets CD4 Antigens Animals Leukocyte Common Antigens |
| Zdroj: | Journal of immunology (Baltimore, Md. : 1950). 161(7) |
| ISSN: | 0022-1767 |
| Popis: | Previous studies have shown that the chronic inflammation observed in the colon of IL-10-deficient (IL-10(-/-)) mice is mediated by CD4+ Th1 T cells and is dependent on the presence of IFN-gamma for its initial development. As CD4+ T cells from IL-10(-/-) mice will cause colitis when transferred into recombinase-activating gene (Rag)-deficient recipients, we considered the possibility that the recipients' NK cells could be an important source of IFN-gamma for the development of colitis. Therefore, the ability of IL-10(-/-) CD4+ T cells to cause colitis in Rag-deficient recipients that had been depleted of NK cells was tested. Contrary to our expectations, NK cell-depleted recipients of IL-10(-/-) CD4+ T cells developed accelerated disease compared with nondepleted recipients. Furthermore, CD4+ T cells from normal mice (IL-10(+/+)) also caused colitis in NK cell-depleted recipient mice, but not in nondepleted recipients. NK cells inhibited effector CD4+CD45RBhigh T cells, and subsequent experiments showed that this effect was dependent on perforin. Thus NK cells can play an important role in down-regulating Thl-mediated colitis by controlling the responses of effector T cells to gut bacteria. |
| Databáze: | OpenAIRE |
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