ArticleFrontiers in immunology2026
PTEN-mTORC2 signaling module controls antibody isotype selection and antiviral humoral immunity.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: The phosphoinositide 3-kinase (PI3K) pathway is a central regulator of activated B cells, yet how PI3K signal strength is interpreted within complex signaling networks to achieve appropriate antibody isotype selection and protective humoral immunity remains incompletely understood. Building on prior work implicating mTOR complexes in germinal center (GC) reactions, we investigated how this circuitry operates under pathological PI3K hyperactivation driven by loss of the PI3K antagonist PTEN. Methods: Using Results: PTEN deficiency impaired IgG1 class switching, a defect selectively rescued by genetic inactivation of mTORC2 but not mTORC1. mTORC2 ablation in PTEN-deficient B cells restored Conclusion: Together, these findings define a PTEN-mTORC2-Akt signaling module within the PI3K network that shapes antibody isotype selection and antiviral humoral immunity, highlighting a potential target for precision modulation of antibody responses in infection, vaccination, and inflammatory diseases.
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