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Cellular immunity is a protective immune process that involves the activation of phagocytes, antigen-sensitized cytotoxic T cells and the release of cytokines and chemokines in response to antigen. Cellular immunity is most effective against cells infected with viruses, intracellular bacteria, fungi and protozoans, and cancerous cells. It also mediates transplant rejection.
Central memory CD8+ T cells (Tcm) are important for lasting anti-tumour immunity and their differentiation is determined by underpinning transcriptional and metabolic regulation. Authors here show that although microwave ablation (MWA) cancer therapy induces T cells to acquire some of the gene expression features of Tcms, but the full metabolic remodeling required for functionality is only achieved if glycolysis is inhibited simultaneously.
Hypoxia induces d-serine production by Mycobacterium tuberculosis which inhibits mTORC1 and T-bet expression to restrict downstream CD8+ T cell immune responses and macrophage activation, and inhibit control of tuberculosis in mice.
Using metabolomics and proteomics data, the quantity and composition of cellular lipid underwent notable changes in different eff Th cell subsets. Especially, Th17 and iTreg cells enhance glycosphingolipid metabolism to sustain their differentiation.
The transient expression of CD61 and its unconventional pairing with CD103 at the immune synapse enhances T cell receptor signaling, improves anti-tumor cytotoxicity and mitigates tumor growth. Clinically, CD61+ tumor infiltrating lymphocytes (TILs) exhibit enhanced effector functions and show limited cellular exhaustion.
A study in Science reports 10 individuals with pre-TCRα deficiency who have late-onset or no clinical phenotype, which suggests that αβ T cells can develop through a pre-TCRα-independent, non-canonical rescue pathway.