Lack of CXCR3 Delays the Development of Hepatic Inflammation but Does Not Impair Resistance to Leishmania donovani

Barbi, Joseph; Oghumu, Steve; Rosas, Lucia E.; Carlson, Tracy; Lu, Bao; Gerard, Craig; Lezama-Davila, Claudio M.; Satoskar, Abhay R.
June 2007
Journal of Infectious Diseases;6/1/2007, Vol. 195 Issue 11, p1713
Academic Journal
CXC chemokine receptor 3 (CXCR3) ligands CXCL9 and CXCL10 are produced at high levels in mice and humans infected with Leishmania donovani, but their contribution to host resistance against L. donovani is not clear. Here, using CXCR3-/- mice, we demonstrate that, although CXCR3 regulates early immune cell trafficking and hepatic inflammation during L. donovani infection, it is not essential for immunity against L. donovani, unlike L. major. CXCR3-/- C57BL/6 mice show a delayed onset of hepatic inflammation and granuloma formation after L. donovani infection. However, they mount an efficient T helper cell type 1 response, recruit T cells to the liver, and control parasite growth as efficiently as do CXCR3+/+ C57BL/6 mice.


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