Different epitopes of the LACK protein are recognized by Vβ4 Vα8 CD4 + T cells in H-2 b and H-2 d mice susceptible to Leishmania major

Abstract

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-γ 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-γ is neutralized. Epitope mapping of LACK protein demonstrated that peptide containing AA 293–305 induced early IL-4 mRNA transcripts in susceptible H-2 b mice i.e. BALB/b and resistant C57BL/6 mice when IFN-γ is neutralized. Stringently, the early IL-4 response to the H-2 d (AA 156–173) or the H-2 b (AA 293–305) epitopes occurred in Vβ4 Vα8 CD4 + T cells from either H-2 d or H-2 b susceptible mice, respectively.