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Posted On: 03/03/2021 10:43:40 AM
Post# of 153907
Interesting quote from the article you referenced:
https://www.nature.com/articles/s41587-020-0602-4
"Because binding of CCL2 or CCL3 to CCR1, CCR2 or CCR5 can induce monocyte recruitment into the lung parenchyma with subsequent differentiation into inflammatory macrophages and consecutive recruitment and activation of additional immune cells and epithelial damage, CCR1, CCR2 and CCR5 might represent promising anti-inflammatory targets in COVID-19. Targeting the CCR2/CCL2 axis has been introduced in HIV and other viral infections53. However, we did not observe CCR2 expression in the respiratory tract of patients with COVID-19 (presumably because of its rapid downregulation in monocytes as they exit the bloodstream and enter tissues; Extended Data Fig. 7), leaving CCR1 and/or CCR5 as potential therapeutic targets.]"
https://www.nature.com/articles/s41587-020-0602-4
"Because binding of CCL2 or CCL3 to CCR1, CCR2 or CCR5 can induce monocyte recruitment into the lung parenchyma with subsequent differentiation into inflammatory macrophages and consecutive recruitment and activation of additional immune cells and epithelial damage, CCR1, CCR2 and CCR5 might represent promising anti-inflammatory targets in COVID-19. Targeting the CCR2/CCL2 axis has been introduced in HIV and other viral infections53. However, we did not observe CCR2 expression in the respiratory tract of patients with COVID-19 (presumably because of its rapid downregulation in monocytes as they exit the bloodstream and enter tissues; Extended Data Fig. 7), leaving CCR1 and/or CCR5 as potential therapeutic targets.]"
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