ReallyPeople?
Good day to all. Thank you for posting this article, good find
and just what I wanted for first weekend read with my hot Colombian coffee at hand …
Our claim to fame is the MOA of Leronlimab. This paper strongly re-enforces Dr. Patterson findings:
In case somebody (still) has any doubts, this comprehensive study using single-cell RNA sequencing on nasopharyngeal and bronchial samples leads to the same place: CCR5. This ads compelling scientific credibility to the conclusion that Dr. Patterson achieved some time back.
And increases our hopes in regards to the clinical trials results.
L & G, the moment of the truth is approaching ... next two weeks will be very interesting. Let's hope CYDY's science will come to our countries' rescue as COVID is spreading like fire.
You all have a great weekend.
Good day to all. Thank you for posting this article, good find
and just what I wanted for first weekend read with my hot Colombian coffee at hand … Our claim to fame is the MOA of Leronlimab. This paper strongly re-enforces Dr. Patterson findings:
Quote:To investigate these questions, we conducted a comprehensive study of mucosal immune responses in patients with COVID-19 that includes samples from both the upper and lower respiratory tract and sequencing data on both immune and epithelial cells. We found that critical disease severity correlates with stronger interactions between epithelial and immune cells and hyperactivated inflammatory macrophages and cytotoxic T lymphocytes, likely contributing to exacerbated epithelial cell death.
Quote:Our data suggest that pharmacologic inhibition of the CCR1 and/or CCR5 pathways might suppress immune hyperactivation in critical COVID-19.
Quote:We found a significant induction of CCL2 and CCL3 expression in macrophages together with an increased expression of CCR1, the receptor for both chemokines, in patients with critical COVID-19. 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.
Quote: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.
In case somebody (still) has any doubts, this comprehensive study using single-cell RNA sequencing on nasopharyngeal and bronchial samples leads to the same place: CCR5. This ads compelling scientific credibility to the conclusion that Dr. Patterson achieved some time back.
And increases our hopes in regards to the clinical trials results.
L & G, the moment of the truth is approaching ... next two weeks will be very interesting. Let's hope CYDY's science will come to our countries' rescue as COVID is spreading like fire.
You all have a great weekend.
9
