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Related Experiment Video

Updated: Jun 3, 2026

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Activated PIK3CD drives marginal zone B cell development from early transitional progenitors by enhancing ADAM10

Ge Lv¹, Yelei Gao², Zhijuan Kang^3,4,5

¹Department of Rheumatology and Immunology, Shenzhen Children's Hospital, Shenzhen, 518000, Guangdong, China.

Inflammation Research : Official Journal of the European Histamine Research Society ... [Et Al.]

|June 2, 2026

Summary

Activated PI3K-delta syndrome (APDS) involves impaired B cell development. This study shows hyperactive PI3Kδ signaling increases marginal zone B cell precursors, offering insights into autoimmune B cell targeting in APDS.

Keywords:

ADAM10 Activated phosphoinositide 3-kinase δ syndrome Marginal zone B cells Progenitor cells scRNA-seq

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Published on: March 7, 2022

Area of Science:

Immunology
Molecular Biology
Genetics

Background:

Activated PI3K-delta syndrome (APDS) is a primary immunodeficiency caused by PIK3CD mutations.
APDS presents with immune dysregulation, including infections and autoimmunity.
Impaired B cell development, particularly marginal zone B cells, is implicated in APDS pathogenesis.

Purpose of the Study:

To investigate the role of PI3Kδ signaling in spleen marginal zone B cell development using a mouse model of APDS.

Main Methods:

Utilized a mouse model of activated PI3Kδ syndrome.
Employed single-cell RNA sequencing (scRNA-seq) to analyze B cell differentiation.
Investigated the effect of an ADAM10 inhibitor on B cell development.

Main Results:

Hyperactive PI3Kδ signaling increases spleen marginal zone B cell precursors with elevated ADAM10 levels at the T1 stage.
scRNA-seq revealed divergent cell differentiation at the T1 stage.
ADAM10 inhibition suppressed marginal zone B cell differentiation and partially corrected T1/T2 stage imbalance.

Conclusions:

Findings elucidate mechanisms of imbalanced marginal zone B cell development in APDS.
Provides a basis for developing strategies to target autoimmune B cells in APDS.