| First Author | Buxbaum LU | Year | 2002 |
| Journal | Eur J Immunol | Volume | 32 |
| Issue | 11 | Pages | 3206-15 |
| PubMed ID | 12555666 | Mgi Jnum | J:115538 |
| Mgi Id | MGI:3691906 | Doi | 10.1002/1521-4141(200211)32:11<3206::AID-IMMU3206>3.0.CO;2-J |
| Citation | Buxbaum LU, et al. (2002) Control of New World cutaneous leishmaniasis is IL-12 independent but STAT4 dependent. Eur J Immunol 32(11):3206-15 |
| abstractText | Leishmania mexicana, a New World protozoan parasite, induces small, chronic, but non-progressive lesions in C57BL/6 (B6) mice. In this study we investigated the role of IL-12, and subsequent Th1 factors, in controlling cutaneous L. mexicana infection. IL-12 treatment failed to promote disease resolution, suggesting that the inability of mice to heal is not related to a deficiency of endogenous IL-12 production. Surprisingly, L. mexicana-induced cutaneous lesions in wild-type and IL-12p40-deficient mice were indistinguishable, with similar parasite burdens, immune responses, and lesion histopathology. In contrast, iNOS, IFN-gamma, and STAT4-deficient mice developed progressive disease and uncontrolled parasite growth. These results differ dramatically from L. major infection, in which IL-12p40-deficient mice are highly susceptible, with very rapid lesion growth, very large parasite burdens, and the development of a strong Th2 response. These data uncover the existence of an alternate IFN-gamma and iNOS pathway for control of Leishmania lesions, which is IL-12 independent, but which unexpectedly requires STAT4. |
