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Matches in SemOpenAlex for { <https://semopenalex.org/work/W4313347773> ?p ?o ?g. }

• W4313347773 endingPage "3130" @default.
• W4313347773 startingPage "3123" @default.
• W4313347773 abstract "Abstract The ability of HIV-1 gp120 to inhibit chemokine signaling prompted us to determine whether signaling through CD4 by a natural ligand, IL-16, could alter cellular responsiveness to chemokine stimulation. These studies demonstrate that IL-16/CD4 signaling in T lymphocytes results in a selective loss of macrophage-inflammatory protein (MIP)-1β/CCR5-induced chemotaxis. There was no effect on monocyte chemoattractant protein-2/CCR1, -2, or -3-induced chemotaxis. Desensitization of CCR5 by IL-16 required at least 10 min of pretreatment; no modulation of CCR5 expression was observed, nor was MIP-1β binding to CCR5 altered. Using murine T cell hybridomas transfected to express native or mutated forms of CD4, it was determined that IL-16/CD4 induces a p56lck-dependent signal that results in desensitization of CCR5. The desensitization process is reciprocal and again selective, as prior CCR5 stimulation, but not CCR1, -2, or -3 stimulation, completely inhibits IL-16/CD4-induced T cell migration. Of interest, while p56lck enzymatic activity is not required for IL-16-induced migration, it was required for desensitization of CCR5. These studies indicate the existence of reciprocal receptor cross-desensitization between CD4 and CCR5 induced by two proinflammatory cytokines and suggest a selective relationship between the two receptors." @default.
• W4313347773 created "2023-01-06" @default.
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• W4313347773 date "1999-09-15" @default.
• W4313347773 modified "2023-10-14" @default.
• W4313347773 title "Reciprocal Desensitization of CCR5 and CD4 Is Mediated by IL-16 and Macrophage-Inflammatory Protein-1β, Respectively" @default.
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• W4313347773 doi "https://doi.org/10.4049/jimmunol.163.6.3123" @default.
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