Brucella abortus lipopolysaccharide in murine peritoneal macrophages acts as a down-regulator of T cell activation
Brucella abortus lipopolysaccharide in murine peritoneal macrophages acts as a down-regulator of T cell activation
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DOI：
10.4049/jimmunol.165.9.5202
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发表时间：
2000-11-01
影响因子：
4.4
通讯作者：
Gorvel, JP
中科院分区：
文献类型：
--
作者：
Forestier, C;Deleuil, F;Gorvel, JP
巨噬细胞通过充当专职吞噬细胞和完全胜任的APC在宿主针对病原体的免疫应答中发挥核心作用。我们在这里报告，LPS从兼性细胞内革兰氏阴性细菌流产布鲁氏菌干扰MHC II类抗原呈递途径。LPS可抑制巨噬细胞向特异性CD4 + T细胞呈递HEL抗原肽的能力，但对OVA向特异性CD8 + T细胞呈递HEL抗原肽的能力无影响。在巨噬细胞的细胞表面，我们观察到高度富集MHC II类分子的LPS大结构域的存在，这可能是显著下调CD4（+）T细胞活化的原因，这种现象可以解释某些细菌病原体对免疫系统的回避，并可以解释慢性布鲁氏菌病患者中观察到的免疫抑制。
Macrophages play a central role in host immune responses against pathogens by acting as both professional phagocytic cells and as fully competent APCs. We report here that the LPS from the facultative intracellular Gram-negative bacteria Brucella abortus interferes with the MHC class II Ag presentation pathway. LPS inhibits the capacity of macrophages to present hen egg lysozyme (HEL) antigenic peptides to specific CD4(+) T cells but not those of OVA to specific CD8(+) T cells, This defect was neither related to a decrease of MHC class II surface expression nor to a deficient uptake or processing of HEL, In addition, B. abortus EPS did not prevent the formation of SDS-resistant MHC class II complexes induced by HEL peptides, At the cell surface of macrophages, we observed the presence of LPS macrodomains highly enriched in MHC class II molecules, which may be responsible for the significant down-regulation of CD4(+) T cell activation, This phenomenon may account for the avoidance of the immune system by certain bacterial pathogens and may explain the immunosuppression observed in individuals with chronic brucellosis.