| First Author | Revaz-Breton M | Year | 2010 |
| Journal | Eur J Immunol | Volume | 40 |
| Issue | 6 | Pages | 1697-707 |
| PubMed ID | 20333623 | Mgi Jnum | J:160950 |
| Mgi Id | MGI:4456340 | Doi | 10.1002/eji.200939821 |
| Citation | Revaz-Breton M, et al. (2010) The MyD88 protein 88 pathway is differently involved in immune responses induced by distinct substrains of Leishmania major. Eur J Immunol 40(6):1697-707 |
| abstractText | Host resistance to Leishmania major is highly dependent on the development of a Th1 immune response. The TLR adaptator myeloid differentiation protein 88 (MyD88) has been implicated in the Th1 immune response associated with the resistant phenotype observed in C57BL/6 mice after infection with L. major. To investigate whether the MyD88 pathway is differentially used by distinct substrains of parasites, MyD88(-/-) C57BL/6 mice were infected with two substrains of L. major, namely L. major LV39 and L. major IR75. MyD88(-/-) mice were susceptible to both substrains of L. major, although with different kinetics of infection. The mechanisms involved during the immune response associated with susceptibility of MyD88(-/-) mice to L. major is however, parasite substrain-dependent. Susceptibility of MyD88(-/-) mice infected with L. major IR75 is a consequence of Th2 immune-deviation, whereas susceptibility of MyD88(-/-) mice to infection with L. major LV39 resulted from an impaired Th1 response. Depletion of regulatory T cells (Treg) partially restored IFN-gamma secretion and the Th1 immune response in MyD88(-/-) mice infected with L. major LV39, demonstrating a role of Treg activity in the development of an impaired Th1 response in these mice. |
