CC chemokine receptor 1 enhances susceptibility to Leishmania major during early phase of infection.

CC chemokine receptor 1 enhances susceptibility to Leishmania major during early phase of infection.
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CC 趋化因子受体 1 在感染早期增强对大型利什曼原虫的易感性。

DOI:
10.1046/j.0818-9641.2002.01132.x
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发表时间:
2003
影响因子:
4
通讯作者:
Satoskar,AbhayR
Satoskar,AbhayR
中科院分区:
医学3区
文献类型:
--
作者:
Rodriguez-Sosa,Miriam;Rosas,LuciaE;Terrazas,LuisI;Lu,Bao;Gerard,Craig;Satoskar,AbhayR

文献摘要

相似文献

CC chemokine receptor 1 (CCR1) is expressed on the surfaces of monocytes, lymphocytes, neutrophils and eosinophils. CC chemokine receptor 1 not only regulates leucocyte chemotaxis, but also plays a role in the regulation of Th1/Th2 cytokine responses. To determine the role of CCR1 in regulation of immune response duringLeishmania majorinfection, we analysed the course of cutaneousL. majorinfection in CCR1‐deficient C57BL/6 mice (CCR1−/−) and compared with similarly infected wild‐type mice (CCR1+/+). FollowingL. majorinfection, CCR1−/− mice developed significantly smaller lesions containing fewer parasites than CCR1+/+ mice. Furthermore, the severity of the inflammation as assessed by the degree of leucocyte infiltration at the site of infection was similar in CCR1+/+ and CCR1−/− mice. Although both groups developed significant antibody responses followingL. majorinfection, CCR1−/− mice produced significantly lower IgE. On day 20 postinfection, LmAg‐stimulated lymph node cells fromL. major‐infected CCR1+/+ and CCR1−/− mice produced comparable levels of IL‐12 and IFN‐γ, but those from CCR1−/− mice produced significantly less IL‐4 and IL‐10. By day 70, lymph node cells from both CCR1+/+ and CCR1−/− mice produced significant amounts of IL‐12 and IFN‐γ but low IL‐4. At both time points, the draining lymph nodes from CCR1+/+ and CCR1−/− mice contained similar number of leucocytes. These results demonstrate that CCR1 plays a role in pathogenesis of cutaneousL. majorinfection. Moreover, they also indicate that CCR1 exacerbatesL. majorinfection in C57BL/6 mice by up‐regulating Th2‐like response rather than inhibiting Th1 development or/and influencing leucocyte chemotaxis.