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Abstract

We previously showed that T cells expressing granzyme (Urn) A are more frequent in skin lesions of susceptible mice than in those of resistant mice infected with the intracellular parasite Leishmania major. To determine the in viva role of gum in cutaneous leishmaniasis, we examined the course of L major infection in gzmA-deficient mice. Despite a delay in host colonization of susceptible mice, the lack of gzmA did not influence the curse of lesion development or result in a discernible iteration of the interferon-γ and interleukin-4 production. Moreover, no differences in these parameters were observed between wild-type controls and mice deficient in gzmB or both gzmA and gzmB. These findings indicate that neither gzmA nor gzmB are critical for the development of T helper cell responses and the outcome of L. major infection.