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15554931, images] [Full Text]" pmid="15554931"Campbell et al.
(2001) determined that T lymphocytes homing to the lung in both normal and asthmatic subjects express CCR5 and CXCR3 but not CCR9 (604738), which is found on T cells homing to intestinal mucosal sites, or CLA (see SELPLG; 600738), which is found on skin-homing T cells. (2003) found that Toxoplasma gondii stimulated Il12 (161560) production not only through a Toll-like receptor/Myd88-dependent mechanism, but also through the release of an 18-k D protein, cyclophilin-18 (C18), that interacted directly with Ccr5 on DCs.
The chemokines studied were generically referred to as MMR, an abbreviation for MIP-1-alpha, MIP-1-beta, and RANTES. (1999) showed that the chemokine receptor CCR5, a principal HIV-1 coreceptor, is posttranslationally modified by O-linked glycosylation and by sulfation of its N-terminal tyrosines.
(1998) found transient natural resistance over time of most of 128 hemophiliacs who were inoculated repeatedly with HIV-1-contaminated factor VIII (300841) concentrate from plasma during 1980 to 1985, before the development of the HIV blood test.
The results suggested that CCR5-positive cells are recruited to inflammatory sites and, as such, may facilitate transmission of macrophage-tropic strains of HIV-1. (1998) found that there were factors other than CCR5 polymorphisms accounting for the fact that exposure to HIV-1 does not usually lead to infection.
Although this fact could be because of insufficient virus titer, there is abundant evidence that some individuals resist infection even when directly exposed to a high titer of HIV.
10089882] [Full Text]" pmid="10089882"Farzan et al. (1999) concluded that tyrosine sulfation may contribute to the natural function of many 7-transmembrane-segment receptors and may be a modification common to primate immunodeficiency virus coreceptors.
The HIV-1 envelope glycoprotein gp120 interacts consecutively with CD4 and the CCR5 coreceptor to mediate the entry of certain HIV-1 strains into target cells.