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Veterans Affairs Hospital and Division of Infectious Diseases, University of Cincinnati College of Medicine, Cincinnati, OH 45267
We determined whether the absence of IL-10 in mice influenced protective and memory immunity to Histoplasma capsulatum. IL-10-/- mice cleared primary and secondary infection more rapidly than wild-type controls. Administration of mAb to TNF-
or IFN-
, but not GM-CSF, abrogated protection in naive IL-10-/- mice; mAb toTNF-, but not IFN- or GM-CSF, subverted protective immunity in secondary histoplasmosis. The inflammatory cell composition in IL-10-/- mice was altered in those given mAb to IFN- or TNF-. More Gr-1+ and Mac-3+ cells were present in lungs of IL-10-/- mice given mAb to IFN-, and treatment with mAb to TNF- sharply reduced the number of CD8+ cells in lungs of IL-10-/- mice. We ascertained whether the lack of IL-10 modulated memory T cell generation or the protective function of cells. The percentage of CD3+, CD44high, CD62low, and IFN-+ cells in IL-10-/- mice was higher than that of wild-type at day 7 but not day 21 or 49 after immunization. Fewer splenocytes from immunized IL-10-/- mice were required to mediate protection upon adoptive transfer into infected TCR 
-/- mice. Hence, deficiency of IL-10 confers a salutary effect on the course of histoplasmosis, and the beneficial effects of IL-10 deficiency require endogenous TNF- and/or IFN-. Memory cell generation was transiently increased in IL-10-/- mice, but the protective function conferred by cells from these mice following immunization is strikingly more vigorous than that of wild-type.
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