The date of this article is January of 2022. It
Post# of 147670
(Total Views: 756)
Posted On: 03/27/2022 11:54:03 AM
The date of this article is January of 2022. It is basic LL related science info. It uncovers NO new insights for the folks on this board. In my biased view the article is but another brick in the LL wall. Another brick in the black letter understanding of the scientific knowledge surrounding CCR 5. By implication and inclusion of LL's MoA in this article it is also a strong commentary on the relevance and importance of LL to the growing and standing scientific knowledge surrounding CCR 5 and inflammation . TAKEAWAY: If the current scientific community cannot and does not ignore LL, neither can big pharma or the FDA. I'll take it.
Excerpt:
Leronlimab, a CCR5-blocking monoclonal antibody, binds to the external domains of CCR5 and through a competitive mechanism prevents HIV and SIV from binding to the CCR5 coreceptor, entering the cell and replication (199, 200). Beside the CCR5 masking from SIV/HIV, leronlimab CCR5 binding does not downregulate CCR5 expression or deplete CCR5-expressing cells (199), but prevents CCL-5-induced activation and migration of inflammatory CCR5-expressing monocytes and T lymphocytes along a chemical gradient (199). In this context, leronlimab appears a an excellent prospect for treatment of diseases, in which the CCL5-CCR5 pathway is involved in the pathogenesis. Given the role of CCR5 in immune cell migration and inflammation, CCR5 blockade with leronlimab was applied in critical COVID-19 patients, and led to the reduction of the IL-6 levels, restoration of CD4/CD8 ratio, and resolution of SARS-CoV-2 burden, thus implicating CCR5 as a potential therapeutic target for COVID-19 (201).
Excerpt:
Leronlimab, a CCR5-blocking monoclonal antibody, binds to the external domains of CCR5 and through a competitive mechanism prevents HIV and SIV from binding to the CCR5 coreceptor, entering the cell and replication (199, 200). Beside the CCR5 masking from SIV/HIV, leronlimab CCR5 binding does not downregulate CCR5 expression or deplete CCR5-expressing cells (199), but prevents CCL-5-induced activation and migration of inflammatory CCR5-expressing monocytes and T lymphocytes along a chemical gradient (199). In this context, leronlimab appears a an excellent prospect for treatment of diseases, in which the CCL5-CCR5 pathway is involved in the pathogenesis. Given the role of CCR5 in immune cell migration and inflammation, CCR5 blockade with leronlimab was applied in critical COVID-19 patients, and led to the reduction of the IL-6 levels, restoration of CD4/CD8 ratio, and resolution of SARS-CoV-2 burden, thus implicating CCR5 as a potential therapeutic target for COVID-19 (201).
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