The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Journal of Experimental Medicine, Vol 165, 546-559, Copyright © 1987 by Rockefeller University Press

ARTICLES

Cutaneous leishmaniasis. The defect in T cell influx in BALB/c mice

MJ McElrath, G Kaplan, A Nusrat and ZA Cohn

Local cellular responses to cutaneous infection with Leishmania mexicana amazonensis were examined in susceptible (BALB/c) and resistant (C57BL/6) mouse strains by immunocytochemical and electron microscopic studies. Infection during the first 8 wk in both animal strains was characterized by progressively enlarging lesions, epidermal thickening and ulceration, and accumulation of eosinophils and Ia+ infected macrophages. Healing of C57BL/6 mouse lesions began after 12 wk of infection and was associated with local influx of both Th (L3T4+) and T cytotoxic/suppressor (Lyt-2+) cells into the dermis, and Ia antigen expression on epidermal keratinocytes. T lymphocyte infiltration was marked and intracellular parasites were scarce by 21 wk of C57BL/6 infection. Similarly, granulomas in C57BL/6 livers contained L3T4+ and Lyt-2+ T lymphocytes and no visible intracellular parasites by 21 wk of infection. In contrast, BALB/c mouse lesions continued to enlarge and never healed. Throughout the entire course of infection, T lymphocyte influx into the heavily infected dermis was minimal. Keratinocyte Ia expression was absent in BALB/c lesions. BALB/c livers were heavily infected by 18 wk of cutaneous infection, with few demonstrable T lymphocytes. A systemic absence of T cells could not be demonstrated in BALB/c mice. Both L3T4+ and Lyt-2+ T cells were found in the peripheral blood in normal numbers in both mouse strains. Our results support the role of T cells as important local effector cells in the healing response of murine cutaneous leishmaniasis. We suggest that local T lymphocyte infiltration may provide lymphokines, particularly IFN-gamma, that can activate infected macrophages to destroy the intracellular parasites. Alternatively, T cells may play a cytotoxic role, killing infected macrophages and allowing local humoral factors to destroy released extracellular parasites.
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