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Immunol Lett. 1993 Jul;37(1):13-7.

Course of Leishmania infection in beta 2-microglobulin-deficient mice.

Author information

1
Max-Planck-Institut für Biologie, Abteilung Membranbiochemie, Tübingen, Germany.

Abstract

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.

PMID:
7901152
DOI:
10.1016/0165-2478(93)90126-m
[Indexed for MEDLINE]

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