ArticleNature immunology2024
PI3Kγ in B cells promotes antibody responses and generation of antibody-secreting cells.
Article in Nature immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Targeting PI3Kδ for lymphoma and immune diseases treatment: a review.Molecular diversity · 2026Review
- Dual targeting of PI3Kγ and STING overcomes regulatory B cell- and myeloid cell-driven immune suppression in pancreatic cancer.Nature cancer · 2026Article
- Causal Links Between Antibody-Mediated Immune Responses and Pancreatic Cancer Risk.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Selective phosphoinositide 3-kinase inhibitors and implication in diabetic retinopathy as pharmacological tools.Frontiers in pharmacology · 2026Review
- CSDE1 depletion inhibits tumor progression through enhancing B-cell infiltration in NSCLC.Cell death & disease · 2025Article
- The role of autoantibodies in bridging obesity, aging, and immunosenescence.Immunity & ageing : I & A · 2024Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
The differentiation of naive and memory B cells into antibody-secreting cells (ASCs) is a key feature of adaptive immunity. The requirement for phosphoinositide 3-kinase-delta (PI3Kδ) to support B cell biology has been investigated intensively; however, specific functions of the related phosphoinositide 3-kinase-gamma (PI3Kγ) complex in B lineage cells have not. In the present study, we report that PI3Kγ promotes robust antibody responses induced by T cell-dependent antigens. The inborn error of immunity caused by human deficiency in PI3Kγ results in broad humoral defects, prompting our investigation of roles for this kinase in antibody responses. Using mouse immunization models, we found that PI3Kγ functions cell intrinsically within activated B cells in a kinase activity-dependent manner to transduce signals required for the transcriptional program supporting differentiation of ASCs. Furthermore, ASC fate choice coincides with upregulation of PIK3CG expression and is impaired in the context of PI3Kγ disruption in naive B cells on in vitro CD40-/cytokine-driven activation, in memory B cells on toll-like receptor activation, or in human tonsillar organoids. Taken together, our study uncovers a fundamental role for PI3Kγ in supporting humoral immunity by integrating signals instructing commitment to the ASC fate.
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Registered trials
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