Lack of CXCR3 delays the development of hepatic inflammation but does not impair resistance to Leishmania donovani.
J Infect Dis
; 195(11): 1713-7, 2007 Jun 01.
Article
en En
| MEDLINE
| ID: mdl-17471442
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.
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Colección:
01-internacional
Base de datos:
MEDLINE
Contexto en salud:
3_ND
Problema de salud:
3_zoonosis
Asunto principal:
Leishmania donovani
/
Receptores de Quimiocina
/
Inflamación
/
Leishmaniasis Visceral
/
Hígado
Límite:
Animals
/
Female
/
Humans
/
Male
Idioma:
En
Revista:
J Infect Dis
Año:
2007
Tipo del documento:
Article
País de afiliación:
Estados Unidos