Lack of CXCR3 delays the development of hepatic inflammation but does not impair resistance to Leishmania donovani

Joseph Barbi, Steve Oghumu, Lucia E. Rosas, Tracy Carlson, Bao Lu, Craig Gerard, Claudio M. Lezama-Oavila, Abhay R. Satoskar

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1713-1717
Number of pages5
JournalJournal of Infectious Diseases
Volume195
Issue number11
DOIs
StatePublished - Jun 1 2007

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

Cite this

Barbi, J., Oghumu, S., Rosas, L. E., Carlson, T., Lu, B., Gerard, C., Lezama-Oavila, C. M., & Satoskar, A. R. (2007). Lack of CXCR3 delays the development of hepatic inflammation but does not impair resistance to Leishmania donovani. Journal of Infectious Diseases, 195(11), 1713-1717. https://doi.org/10.1086/516787