Control of Infection withLeishmania majorin Susceptible BALB/c Mice Lacking the Common γ-Chain for FcR Is Associated with Reduced Production of IL-10 and TGF-β by Parasitized Cells
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Media type:
E-Article
Title:
Control of Infection withLeishmania majorin Susceptible BALB/c Mice Lacking the Common γ-Chain for FcR Is Associated with Reduced Production of IL-10 and TGF-β by Parasitized Cells
Contributor:
Padigel, Udaikumar M.;
Farrell, Jay P.
Published:
The American Association of Immunologists, 2005
Published in:
The Journal of Immunology, 174 (2005) 10, Seite 6340-6345
Language:
English
DOI:
10.4049/jimmunol.174.10.6340
ISSN:
0022-1767;
1550-6606
Origination:
Footnote:
Description:
AbstractPrevious studies have shown that the in vitro ligation of FcγRs with IgG-opsonized Leishmania amastigotes promotes IL-10 production by macrophages. In addition, infection of either BALB/c mice lacking the common γ-chain of Fc receptors (FcγR−/−) or mice genetically altered to lack circulating Ab (JHD) with Leishmania pifanoi results in reduced and delayed lesion development and a deficit in the recruitment of inflammatory cells into infected lesions. We show in this study that FcγR−/− mice can control infection with Leishmania major and totally resolve cutaneous lesions. The ability to eventually control infection is not associated with a reduction in lesion inflammation or a reduction in the ability of Leishmania to parasitize cells through week 6 of infection. The immune response in healing FcγR−/− mice is associated with a reduction in numbers of cells producing Th2-type cytokines, including IL-4 and IL-10, but not an increase in numbers of IFN-γ-producing cells characteristic of a dominant Th1-type response. Instead, we observe a reduction in levels of IL-10 and TGF-β within infected lesions, including reduced levels of these cytokines within parasitized macrophages. Together, these results suggest that uptake of opsonized parasites via FcγRs may be a strong in vivo stimulus for the production of anti-inflammatory cytokines that play a role in susceptibility to infection.