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RESISTANCE AND ABROGATION OF RESISTANCE TO CUTANEOUS LEISHMANIASIS IN RECONSTITUTED BALB/c NUDE MICE
Author(s) -
Mitchell Graham F,
Curtis Joan M,
Scollay Roland G,
Handman Emanuela
Publication year - 1981
Publication title -
australian journal of experimental biology and medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0004-945X
DOI - 10.1038/icb.1981.47
Subject(s) - spleen , immunology , balb/c , lymph node , biology , immune system , cutaneous leishmaniasis , leishmania major , lymph , leishmaniasis , microbiology and biotechnology , leishmania , pathology , medicine , parasite hosting , world wide web , computer science
Summary Normal BALB/c mice and hypothymic BALB/c nude mice are highly susceptible to infection with an isolate of the intramacrophage protozoan parasite, Leishmania tropica , developing severe cutaneous disease. Nude mice reconstituted with large numbers of BALB/c lymphoid cells are also susceptible but are resistant when injected with low numbers of cells (e.g. 5 × 10 6 spleen plus mesenteric lymph node cells). Susceptibility to chronic cutaneous disease is thus quite different in minimally reconstituted BALB/c nude mice than in BALB/c mice with a normal or near‐normal complement of T cells. Recovered minimally reconstituted nudes are susceptible to reinfection but, again, lesions heal. The minimally reconstituted, resistant nude mouse has been used as a screen for cellular and serum components which may contribute to chronicity of cutaneous disease in infected BALB/c mice. low numbers of T cell‐enriched spleen cells from chronically infected BALB/c mice are not protective in nude mice and, in fact, abrogate the protective effect of low numbers of syngeneic normal mouse spleen cells in a mix experiment. Treatment of chronically infected mouse spleen cells with anti‐ly2 reagents does not affect the capacity of the cells to abrogate resistance. A proportion of minimally reconstituted nude mice were susceptible to cutaneous disease after multiple injections of serum from chronically infected mice. However, this abrogation of resistance differed from that mediated by cells of chronically infected mice in being inconsistent. The results suggest that T cell‐dependent immune responses (but perhaps not Ly2 + T 8 cell‐dependent effects) contribute to chronicity of infection in genetically susceptible BALB/c mice and inhibit healing of lesions in this mouse strain. Although the possibility is raised by the data, no compelling evidence was obtained in this series of experiments that T H cell‐dependent ‘blocking antibodies’, or other serum components, are involved in perpetuating chronic disease in BALB/c mice.