Researchers find that the deletion of Gα13 in B-cells increases lymphoma risk by enhancing proliferation in gut-associated lymph nodes. Dietary glutamine significantly promotes these effects, highlighting a crucial link between diet and cancer.
By Pooja Toshniwal PahariaReviewed by Benedette Cuffari, M.Sc.Jul 29 2024 In a recent study published in the journal Nature Immunology , researchers investigate the effects of microenvironment signals on selection in mucosal germinal centers and their role in the development of B-cell lymphomas.
Chronic GCs can develop due to influences from the gut microbiota and nutrition. However, it remains unclear what specific dietary factors are involved in mucosal GCs. Cellular signaling pathways mediated by Gα13 lead to reduced cellular migration, which subsequently confines GCBs to B-cell niches such as the bone marrow, secondary lymphoid organs, GCs, and peripheral tissues. Gα13 activity can also prevent the accumulation of B-cells in GCs, which may be mediated by the inhibition of phosphatidylinositol-3 kinase /protein kinase B .
Gna13f/f mice were crossbred with those possessing GC-specific tamoxifen-inducible fate reporter alleles to investigate whether Gα13 loss resulted in an increased mutational burden due to the sustained residence of Gα13-deficient clones in the mesenteric lymph node germinal centers. The researchers evaluated the mechanistic target of rapamycin complex 1 signaling in Gα13-deficient cells, depleted cluster of differentiation 4-expressing cells, and intestinal lymph-derived molecules. They also measured mLN GCB counts and Myc proto-oncogene expression in control and Gα13 knockout bone marrow chimeras. They also examined the role of glutamine transport proteins in the depletion of Gα13 in mLN GCBs.
Gα13-deficient GCBs appear to have a competitive advantage, as they can successfully grow in mLNs without T-cell support or influence from the gut microbiome. Loss of Gα13-mediated inhibitory signaling on mTORC1 signaling and Myc expression may enhance T-cell-independent refueling of Gα13-deficient GCBs, thus leading to competitive proliferation and clonal persistence in the GC state.
Glutamine Lymphoma Antigen Bone Bone Marrow Chronic Genetic Immunology Kinase Lymph Node Lymph Nodes Nutrition Oncogene Proliferation Protein Rapamycin Receptor Research T-Cell
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