Different epitopes of the LACK protein are recognized by V beta 4 V alpha 8 CD4+ T cells in H-2b and H-2d mice susceptible to Leishmania major.


Autoria(s): Launois P.; Pingel S.; Himmelrich H.; Locksley R.; Louis J.
Data(s)

2007

Resumo

After inoculation of Leishmania major, a rapid production of IL-4 by LACK-specific CD4+ T cells has been shown to drive Th2 cell development in susceptible mice i.e. BALB/c and C57BL/6 mice rendered susceptible by neutralization of IFN-gamma at the onset of infection. Here, we showed that peptide AA 156-173 induced an early IL-4 mRNA expression not only in BALB/c mice but also in resistant B10.D2 mice when IFN-gamma is neutralized. Epitope mapping of LACK protein demonstrated that peptide containing AA 293-305 induced early IL-4 mRNA transcripts in susceptible H-2b mice i.e. BALB/b and resistant C57BL/6 mice when IFN-gamma is neutralized. Stringently, the early IL-4 response to the H-2d (AA 156-173) or the H-2b (AA 293-305) epitopes occurred in V beta 4 V alpha 8 CD4+ T cells from either H-2d or H-2b susceptible mice, respectively.

Identificador

http://serval.unil.ch/?id=serval:BIB_27D117601478

isbn:1286-4579 (Print)

pmid:17890126

doi:10.1016/j.micinf.2007.05.017

isiid:000250948900003

Idioma(s)

en

Fonte

Microbes and Infection, vol. 9, no. 11, pp. 1260-1266

Palavras-Chave #Animals; Antigens, Protozoan/immunology; CD4-Positive T-Lymphocytes/immunology; Epitopes/immunology; Female; Gene Expression; Interleukin-4/biosynthesis; Interleukin-4/genetics; Leishmania major/immunology; Leishmaniasis, Cutaneous/immunology; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Protozoan Proteins/immunology; RNA, Messenger/biosynthesis; Receptors, Antigen, T-Cell/immunology; T-Lymphocyte Subsets/immunology; Up-Regulation
Tipo

info:eu-repo/semantics/article

article