The development of effector T cell subsets in murine Leishmania major infection

Leishmania major infection has proven an exceptional model for CD4+ subset development in inbred mice. Most strains contain infection coincident with the appearance of T helper 1 (Th1) cells that produce gamma-interferon (IFN-gamma) required for macrophage activation. In contrast, mice on the BALB b...

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Vydáno v:Ciba Foundation symposium Ročník 195; s. 110
Hlavní autoři: Locksley, R M, Wakil, A E, Corry, D B, Pingel, S, Bix, M, Fowell, D J
Médium: Journal Article
Jazyk:angličtina
Vydáno: Netherlands 01.01.1995
Témata:
Animals
CD4-Positive T-Lymphocytes - immunology
Humans
Leishmania major - immunology
Leishmaniasis, Cutaneous - immunology
T-Lymphocyte Subsets - immunology
ISSN:0300-5208
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Shrnutí:Leishmania major infection has proven an exceptional model for CD4+ subset development in inbred mice. Most strains contain infection coincident with the appearance of T helper 1 (Th1) cells that produce gamma-interferon (IFN-gamma) required for macrophage activation. In contrast, mice on the BALB background are unable to control infection due to the development of Th2 cells that produce counter-regulatory cytokines, particularly interleukin 4 (IL-4), capable of abrogating the effects of IFN-gamma. Selective gene disruption studies in mice have illustrated critical components of the host response to L. major. Mice deficient in beta 2 microglobulin, which have no major histocompatibility complex (MHC) class I or CD8+ T cells, control infection as well as wild-type mice, whereas mice deficient in MHC class II (and CD4+ T cells) suffer fatal infection. Mice with disruption of the gene coding IFN-gamma are also incapable of containing infection, reflecting absolute requirements for this cytokine. A number of interventions have been demonstrated to abrogate Th2 cell development in BALB mice, enabling these mice to control infection. Each of these--IL-12, anti-IL-4, anti-IL-2, anti-CD4 and CTLA4-Ig--has in common the capacity to make IL-4 rate limiting at the time of CD4+ cell priming.
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ISSN:0300-5208
DOI:10.1002/9780470514849.ch8