Cytokines in parasitic diseases: the example of cutaneous leishmaniasis.

Details

Serval ID
serval:BIB_EE545628A1C9
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Title
Cytokines in parasitic diseases: the example of cutaneous leishmaniasis.
Journal
International Reviews of Immunology
Author(s)
Launois P., Tacchini-Cottier F., Parra-Lopez C., Louis J.A.
ISSN
0883-0185 (Print)
ISSN-L
0883-0185
Publication state
Published
Issued date
1998
Volume
17
Number
1-4
Pages
157-180
Language
english
Abstract
The essential role of cytokines in parasitic diseases has been emphasised since the in vivo description of the importance of T helper 1 (Th1) and T helper 2 (Th2) CD4+ T cell responses in resistance and susceptibility to infection with L. major in mice. Th1 cells produced IL-2, IFN-gamma and Lymphotoxin T (LT) and Th2 cells produce IL-4, IL-5 and IL-13. In this model of infection the correlation between on the one hand resistance to infection and the development of a Th1 response and on the other hand susceptibility and Th2 cell development allowed the identification of the mechanisms directing the differentiation of CD4+ T cell precursors towards either Th1 type or Th2 type responses. Cytokines are the crucial inducer of functional CD4+ T cell subset differentiation during infection with L. major. IL-12 and IFN-gamma direct the differentiation of Th1 response and IL-4 of a Th2 response. In susceptible mice, careful analysis of IL-4 production during the first days of infection has shown that the IL-4 produced as a result of a very early burst of IL-4 mRNA expression (16 hours) plays a essential role in the maturation of a Th2 CD4+ T cell response by rendering the CD4+ T cell precursors unresponsive to IL-12. Activation of a restricted population of CD4+ T cells expressing the V beta 4 V alpha 8 TCR heterodimer after recognition of a single antigen, the LACK (Leishmania Activated c Kinase) antigen, resulted in this rapid production of IL-4 required for the subsequent CD4+ T cell differentiation. Thus, tolerization of these cells might contribute a strategy for preventing infection with L. major.
Keywords
Animals, CD4-Positive T-Lymphocytes/immunology, Cytokines/immunology, Disease Models, Animal, Leishmania major/immunology, Leishmaniasis, Cutaneous/immunology, Mice
Pubmed
Create date
24/01/2008 15:09
Last modification date
20/08/2019 16:15
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