T cell-myeloid reprogramming overcomes immune resistance in colorectal cancer models
By
Guillaume Mestrallet1 Send email to [email protected]
Summary
This article presents a scientific study on colorectal cancer (CRC) immunotherapy resistance. It shows that during anti-PD-1 treatment, tumor control is associated with colocalization of specific macrophage subtypes (MHC+ C1Q+ CXCL9+) and T cell subtypes (TCF+ PRF1+). Resistance correlates with increased expression of immune checkpoints TIM3, LAG3, TIGIT, and PD-1. The research demonstrates that targeting TREM2 macrophages alongside LAG3, CTLA4, and PD-1 reprograms the tumor microenvironment and drives antitumor immunity, achieving up to 100% tumor clearance in mismatch repair-deficient models and over 70% in mismatch repair-proficient models.
Source
bskyT cell-myeloid reprogramming overcomes immune resistance in colorectal cancer modelscell.comKey quotes
· 5 pulledMestrallet et al. show that T cell-myeloid interactions determine response to PD-1 blockade in colorectal cancer.
Targeting TREM2 macrophages together with LAG3, CTLA4, and PD-1 reprograms the tumor microenvironment and drives antitumor immunity.
Achieving up to 100% tumor clearance in mismatch repair-deficient and >70% in mismatch repair-proficient models.
Tumor control during anti-PD-1 treatment associates with colocalization of MHC+ C1Q+ CXCL9+ macrophages and TCF+ PRF1+ T cells.
Resistance correlates with increased TIM3, LAG3, TIGIT, and PD-1 expression.
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