19 Facts About CCR5

C-C chemokine receptor type 5, known as CCR5 or CD195, is a protein on the surface of white blood cells that is involved in the immune system as it acts as a receptor for chemokines.

CCR5 protein belongs to the beta chemokine receptors family of integral membrane proteins.

CCR5 is predominantly expressed on T cells, macrophages, dendritic cells, eosinophils, microglia and a subpopulation of either breast or prostate cancer cells.

The expression of CCR5 is selectively induced during the cancer transformation process and is not expressed in normal breast or prostate epithelial cells.

Recent studies suggest that CCR5 is expressed in a subset of cancer cells with characteristics of cancer stem cells, which are known to drive therapy resistance, and that CCR5 inhibitors enhanced the number of cells killed by current chemotherapy.

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Modulation of CCR5 activity contributes to a non-pathogenic course of infection with Simian immunodeficiency virus in several African non-human primate species that are long-term natural hosts of SIV and avoid immunodeficiency upon the infection.

CCR5 is the primary co-receptor used by gp120 sequentially with CD4.

CCR5 is essential for the spread of the R5-strain of the HIV-1 virus.

Unlike CCR5, which is not required, CD4 is critical in the body's immune defense system.

The induction of CCR5 expression promotes cellular invasion, migration, and metastasis.

CCR5 inhibitors including maraviroc and leronlimab have been shown to block lung metastasis of human breast cancer cell lines.

In preclinical studies of immune competent mice CCR5 inhibitors blocked metastasis to the bones and brain.

CCR5 ?32 is a 32-base-pair deletion that introduces a premature stop codon into the CCR5 receptor locus, resulting in a nonfunctional receptor.

Individuals homozygous for CCR5 ?32 do not express functional CCR5 receptors on their cell surfaces and are resistant to HIV-1 infection, despite multiple high-risk exposures.

The idea that negative selection played a role in the allele's low frequency is supported by experiments using knockout mice and Influenza A, which demonstrated that the presence of the CCR5 receptor is important for efficient response to a pathogen.

Hypothesis that smallpox exerted positive selection for CCR5 ?32 is biologically plausible, since poxviruses, like HIV, enter white blood cells using chemokine receptors.

Whether CCR5 function is helpful or harmful in the context of a given infection depends on a complex interplay between the immune system and the pathogen.

Patients homozygous for CCR5 ?32 were found to be at higher risk for a neuroinvasive form of tick-borne encephalitis .

Genetic approach involving intrabodies that block CCR5 expression has been proposed as a treatment for HIV-1 infected individuals.