Response to Chemotherapy in Experimental Visceral Leishmaniasis: T Cell-Dependent but Interferon-γ- and Interleukin-2-Independent

• Published in: The Journal of infectious diseases 1991-03, Vol.163 (3), p.622-624
• Main Authors: Murray, Henry W., Granger, Angela M., Mohanty, Sujit K.
• Format: Article
• Language: English
• Subjects: Animals; Antibodies, Monoclonal; Antimony; Antimony - therapeutic use; Chemotherapy; Disease Models, Animal; Female; Infections; Interferon-gamma - physiology; Interleukin-2 - physiology; Interleukins; Leishmania donovani; Leishmaniasis, Visceral - drug therapy; Leishmaniasis, Visceral - immunology; Liver; Major Articles; Mice; Mice, Inbred BALB C; Parasite hosts; Parasites; T lymphocytes; T-Lymphocytes - physiology; Visceral leishmaniasis
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1093/infdis/163.3.622

The capacity of Leishmania donovani-infected BALB/c mice to respond to conventional chemotherapy with pentavalent antimony (Sb) is T cell dependent and, in nude mice, can be restored in part by treatment with the T celllymphokines, interferon-γ (IFN-γ) or interleukin-2 (IL-2). Todocument the presumed role of endogenous IFN-γand IL-2 in responsiveness to antileishmanial chemotherapy in the T cell-intact host, L. donovani-infected euthymic BALB/c mice were treated with anti-IFN-γ or anti-IL-2 monoclonal antibodies (MAbs)before and after Sb administration. Treatment with MAbs exacerbated visceral infection but did not inhibit the in vivo efficacy of Sb. Thus, while combination therapy of Sb plus IFN-γ or IL-2 may prove beneficial in T cell-deficient hosts with visceral leishmaniasis, T cell activities other than or in addition to IFN-γor IL-2 production may mediate in vivo responsiveness to antileishmanial chemotherapy in the euthymic host.