| First Author | Buxbaum LU | Year | 2015 |
| Journal | Infect Immun | Volume | 83 |
| Issue | 4 | Pages | 1366-71 |
| PubMed ID | 25605773 | Mgi Jnum | J:229278 |
| Mgi Id | MGI:5751370 | Doi | 10.1128/IAI.02909-14 |
| Citation | Buxbaum LU (2015) Interleukin-10 from T cells, but not macrophages and granulocytes, is required for chronic disease in Leishmania mexicana infection. Infect Immun 83(4):1366-71 |
| abstractText | Chronic cutaneous disease of mice caused by the protozoan parasite Leishmania mexicana requires interleukin-10 (IL-10) and FcgammaRIII (an activating IgG receptor). Macrophages readily secrete IL-10 in response to IgG-coated amastigotes, making macrophages a prime candidate as the critical source of IL-10. However, indirect evidence suggested that macrophage IL-10 is not essential for chronic disease. I now show directly that mice lacking IL-10 from macrophages and granulocytes still have chronic disease, like wild-type C57BL/6 mice. However, T cell-derived IL-10 is required for chronic disease. CD4-cre IL-10flox/flox mice lack IL-10 from T cells (both CD4+ and CD8+) and heal their L. mexicana lesions, with parasite control. I had previously shown that depletion of CD25+ T cells had no effect on chronic disease, and thus, T cells other than CD25+ regulatory T (Treg) cells should be the important source of IL-10. Given that conventional T cells do not express FcgammaRs, there is likely to be an indirect pathway by which FcgammaRIII on some other cell engaged by IgG1-amastigote immune complexes induces IL-10 from T cells. Further work is needed to delineate these pathways. |
