chemokine and chemokine receptors show several variations which may affect resistance to infectious disease. a 32 base pair deletion in the open reading frame of the human ccr5 gene (ccr5?32) results in producing a truncated antigen which fails to be presented on the surface of target cells. ccr5?32 variant is not a functional co receptor for hiv-1 entrance and delay the onset of acquired immun...

Chemokine receptor tyrosine sulfation plays a key role in the binding of chemokines. It has been suggested that is heterogeneous, but no experimental evidence provided so far. The potent anti-HIV chemokine analog 5P12-RANTES proposed to owe its inhibitory activity capacity bind larger pool cell surface CCR5 receptors than native chemokines such as CCL5, molecular details underlying this phenome...

Ligands of CCR5, the major coreceptor of HIV-1, costimulate T lymphocyte activation. However, the full impact of CCR5 expression on T cell responses remains unknown. Here, we show that compared with CCR5(+/+), T cells from CCR5(-/-) mice secrete lower amounts of IL-2, and a similar phenotype is observed in humans who lack CCR5 expression (CCR5-Delta32/Delta32 homozygotes) as well as after Ab-me...

BACKGROUND This study aimed to examine how CC chemokine receptor 5 (CCR5) inhibitors (aplaviroc [APL], TAK779 and maraviroc [MVC]) interact with CCR5 and affect its dynamics and physiological CC-chemokine-CCR5 interactions. METHODS A yellow fluorescent protein (YFP)-tagged CCR5-expressing U373-MAGI cell line was generated and a stable CCR5-expressing clonal population, (YFP)CCR5-UM16, was pre...

We have shown that mice that express the C-C chemokine receptor 5 (CCR5) have enhanced local tumor growth and an impaired response to vaccine therapy compared with CCR5 knockout (CCR5(-/-)) mice. Here, we extend these observations to evaluate the function of CCR5 in pulmonary metastasis and the mechanism underlying the diminished tumor growth in CCR5(-/-) mice. Lung metastases were counted in w...

The requirement of human immunodeficiency virus (HIV)-induced CCR5 activation for infection by R5 HIV type 1 (HIV-1) strains remains controversial. Ectopic CCR5 expression in CD4(+)-transformed cells or pharmacological inhibition of G(alpha)i proteins coupled to CCR5 left unsolved whether CCR5-dependent cell activation is necessary for the HIV life cycle. In this study, we investigated the role...