The CCR5 receptor
appears to play a central role in modulating immune cell trafficking to sites of inflammation and may be important in the development of acute graft-versus-host disease (GvHD) and other inflammatory conditions.
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Replacing immune cells with those that don't have the CCR5 receptor
appears to be key in preventing HIV from rebounding after the treatment.
But a very small number of people who are resistant to HIV have two mutated copies of the CCR5 receptor
. This means the virus cannot penetrate cells in the body that it normally infects.
LPS induces CCR5 receptor
expression via the EGFR, COX-2 and ERK1/2 pathways
The CCR5 receptor
is a major entry site for macrophage-tropic (CCR5 tropic) HIV-1 strains into host cells.
Altering CCR5 receptor
will help disable the virus' ability to use T-cells to infect humans.
One of the chemokines that uses the CCR5 receptor
to recruit macrophages to the inflammatory site is CCL3.
Based on these observations, the antiretroviral drug Maraviroc has been used as it is a CCR5 receptor
antagonist, thereby blocking the HIV protein from associating with the receptor.
"One thing that we've lacked is a high-resolution molecular ' picture' of the CCR5 receptor
structure that we can use for precise drug design," Beili Wu, professor at the Chinese Academy of Shanghai Institute of Materia Medica, part of the Chinese Academy of Sciences, said in a statement.
Today the mutation can be found in [approximately equal to]10% of all those of northern European descent, preventing expression of the as-yet mostly inscrutable CCR5 receptor
on the surface of many different subsets of immune cells.