| First Author | Overath P | Year | 1993 |
| Journal | Immunol Lett | Volume | 37 |
| Issue | 1 | Pages | 13-7 |
| PubMed ID | 7901152 | Mgi Jnum | J:14325 |
| Mgi Id | MGI:62496 | Doi | 10.1016/0165-2478(93)90126-m |
| Citation | Overath P, et al. (1993) Course of Leishmania infection in beta 2-microglobulin-deficient mice. Immunol Lett 37(1):13-7 |
| abstractText | Mice homozygous for a beta 2-microglobulin (beta 2-m) gene disruption lack the beta 2-m protein and are deficient in functional major histocompatibility complex class I (MHC I) molecules. The mutant mice have normal numbers of CD4+8- T helper cells but lack MHC I-directed CD4-8+ alpha/beta T cells. The beta 2-m mutant and wild-type mice were infected with Leishmania major or L. mexicana, which cause cutaneous leishmaniasis in the Old and New World, respectively. In both mutant and wild-type mice, the infection with L. major was controlled at a low level of parasitization, while L. mexicana caused a progressive disease. Assuming the absence of compensatory mechanisms, it is concluded that MHC I-directed CD8+ T cells are not important for the course of a Leishmania infection, supporting the prevailing view that control or exacerbation of the disease is modulated by type 1 (TH1) or type 2 (TH2) CD4+8- T cells, respectively. |
