| First Author | Zhou Y | Year | 1998 |
| Journal | J Immunol | Volume | 160 |
| Issue | 8 | Pages | 4018-25 |
| PubMed ID | 9558111 | Mgi Jnum | J:46941 |
| Mgi Id | MGI:1202256 | Doi | 10.4049/jimmunol.160.8.4018 |
| Citation | Zhou Y, et al. (1998) Impaired macrophage function and enhanced T cell-dependent immune response in mice lacking CCR5, the mouse homologue of the major HIV-1 coreceptor. J Immunol 160(8):4018-25 |
| abstractText | The CC-chemokine receptor CCR5 has been shown to be the major coreceptor for HIV-1 entry into cells, and humans with homozygous mutation in the ccr5 gene are highly resistant to HIV-1 infection, despite the existence of many other HIV-1 coreceptors. To investigate the physiologic function of CCR5 and to understand the cellular mechanisms of these clinical observations, we generated a CCR5-deficient mouse model (ccr5[-/-]) by targeted deletion of the ccr5 gene. We found that although developed normally in a pathogen-free environment, CCR5-deficient mice showed reduced efficiency in clearance of Listeria infection and exert a protective effect against LPS-induced endotoxemia, reflecting a partial defect in macrophage function. In addition, CCR5-deficient mice had an enhanced delayed-type hypersensitivity reaction and increased humoral responses to T cell- dependent antigenic challenge, indicating a novel role of CCR5 in down-modulating T cell-dependent immune response. |
