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Re: NY1972 post# 128

Sunday, 05/22/2022 1:29:54 PM

Sunday, May 22, 2022 1:29:54 PM

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I think you mentioned B2M going back. I know one group made a recombinant adenovirus carrying the gene and demonstrated recovery of HLA-I expression on cancer cells deficient in that. This lead to destruction by CD8+ T-cells https://onlinelibrary.wiley.com/doi/10.1111/j.1365-3083.2009.02276.x https://www.nature.com/articles/cgt201432

So that is one way. As for Tregs, ''In mice and humans, CCR8+ Tregs constituted 30 to 80% of tumor Tregs in various cancers and less than 10% of Tregs in other tissues, whereas most tumor-infiltrating conventional T cells (Tconvs) were CCR8–. CCR8+ tumor Tregs were highly differentiated and functionally stable.'' https://www.pnas.org/doi/10.1073/pnas.2114282119

The reason I mention that is due to a few anti-CCR8 mAbs in the clinic. So are anti-CD25 and anti-GARP mAbs https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7116816/ https://aacrjournals.org/cancerres/article/81/13_Supplement/1847/667728/Abstract-1847-Anti-GARP-antibody-DS-1055a-augments
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