Regulation of Cell-Mediated Immunity in Leishmaniasis
Leishmaniasis is caused by species of the intracellular protozoan parasite belonging to the genus Leishmania. There are three main categories of leishmaniasis: cutaneous leishmaniasis (oriental sore), mucocutaneous leishmaniasis (espundia) and visceral leishmaniasis (kala azar). An incidence rate of 400 000 new cases per year has been reported, and the world wide prevalence of leishmaniasis is estimated to be 12 million cases (MODABBER 1987). Visceral leishmaniasis is fatal if not treated. The last epidemic of leishmaniasis that occurred in India in 1977-1978 caused an estimated 20 000 deaths. Most forms of leishmaniasis are zoonotic, and humans are infected only secondarily. Animal reservoirs of species pathogenic to man include the sloth, dog and rodent. The parasites are transmitted by female sandflies, and the flagellated promastigotes develop in the gut of the sandfly and in cell-free cultures. Transformation into the amastigote stage occurs within the mammalian macrophage. Primary drug treatment is based on antimony compounds, notably the pentavalent antimonials sodium stibogluconate and N-methylglucamine antimonate. These must be given in daily intramuscular doses for several weeks; they entail unpleasant side effects and are not very effective against cutaneous leishmaniasis. The only immunisation strategy against leishmaniasis used so far with any success in man has been restricted to the cutaneous diseases. It is based on convalescent immunity following controlled induction of a lesion with viable L. major (GREENBLATT 1980). The feasibility of vaccination with killed vaccines is currently being evaluated.
KeywordsSugar Interferon Cyclosporin Arena Antimony
Unable to display preview. Download preview PDF.
- Ciliari E, Liew FY, Lelchuk R (1986) Suppression of interleukin-2 production by macrophages in susceptible BALB/c mice infected with Leishmania major. Infect Immun 54: 386–394.Google Scholar
- Greenblatt CL (1980) The present and future of vaccination for cutaneous Leishmaniasis. In: Mizrahi A, Hertman I, Klinberg MA (eds) New developments with human and veterinary vaccines. Liss, New York, p 259–285.Google Scholar
- Howard JG, Hale C, Liew FY (1981) Immunological regulation of experimental cutaneous leishmaniasis. IV. Prophylactic effect of sublethal irradiation as a result of abrogation of suppressor T cell generation in mice genetically susceptible to Leishmania tropica infection. J Exp Med 153: 557–568.PubMedCrossRefGoogle Scholar
- Louis JA, Mendonca S, Titus RG, Cerottini JC, Cerny A, Zinkernagel R, Milon G, Marchai G (1986) The role of specific T cell subpopulations in murine cutaneous leishmaniasis. In: Cinader B, Miller RG (eds) Progress in immunology. VI. Academic, New York, p 762–769.Google Scholar
- Maue J, Behin R (1982) Leishmaniasis. In: Cohen S, Warren KS (eds) Immunology of parasitic infections. Blackwell, p 299-335.Google Scholar
- Modabber F (1987) The leishmaniasis. In: Maurice J, Pearce AM (eds) Tropical disease research, a global partnership, eighth programme report, TDR. World Health Organisation, Geneva, p 99–112.Google Scholar
- Mossmann TR, Cherwinski H, Bond MW, Giedlin MA, Coffman RL (1986) Two types of murine helper T cell clone. I. Definition according to profiles of lymphokine activities and secreted proteins. J Immunol 136: 2348–2357.Google Scholar
- Scott P, Pearce E, Natovitz P, Sher A (1988b) Adoptive transfer of protective immunity against lethal Leishmania major infection with an L3T4 (Thl) T cell clone recognising a low molecular weight parasite antigen. FASEB J 2: Al256.Google Scholar
- Solbach W, Forberg K, Kammerer E, Bogdan C, Rollinghoff M (1986) Suppressive effect of cyclosporin A on the development of Leishmania tropica-induced lesions in genetically susceptible BALB/c mice J. Immunol 137: 702–707.Google Scholar
- Sterm JJ, Oca MJ, Rublin BY, Anderson SL, Murray HW (1988) Role of L3T4+ and Lyt-2+ cells in experimental visceral leishmaniasis. J Immunol 140: 3971–3977.Google Scholar
- Titus R, Kinsey P, Thoedos C, Louis J (1988) Induction of resistance to experimental cutaneous leishmaniasis in genetically-susceptible BALB/c mice by immunisation with chemically-mutagenised non-infective clones of Leishmania major. FASEB J 2: A887.Google Scholar