T-Cell Subsets and T-Cell Antigens in Protective Immunity Against Experimental Leishmaniasis

Abstract

Leishmaniasis is a chronic protozoal infection of man found in South and Central America, Mexico, Africa, Asia, and Europe. The parasite life cycle involves two forms, promastigotes and amastigotes. Promastigotes, found within the sandfly vector, initiate infection by invading macrophages. Once inside macrophages, promastigotes rapidly transform to the nonflagellated amastigote stage, which multiplies intracellularly. Eventually the infected cells rupture, and amastigotes reinvade other macrophages. The ensuing infection can manifest itself in a variety of ways, ranging from healing cutaneous lesions to non-healing cutaneous or visceral infections. This spectral nature is due, in part, to the host’s immunologic response. Thus, although the various species of Leishmania exhibit significant differences, most species appear to be able to produce an inapparent, healing, or nonhealing infection. For example, although the visceral species of Leishmania have long been considered to produce a fatal infection in the absence of drug treatment, it is now known that these parasites may also produce relatively benign cutaneous lesions or completely inapparent infections (BADARO et al. 1986). Similarly, L. braziliensis species often produce a healing cutaneous lesion, although in a small percentage of patients severe mucocutaneous lesions develop.