CD30 influences germinal center B-cell dynamics and local iBALT generation in chronic lung disease

CD30 is a cell surface receptor belonging to the tumor necrosis factor receptor (TNFR) superfamily that was originally identified as a Hodgkin lymphoma marker. Under physiological conditions, CD30 expression is largely confined to a minor B cell population, however, marked expansion of CD30 + B cells have been reported in the context of immune dysregulation and viral infection. Utilizing conditional CD30-knockin mouse strains we were able to investigate the role of CD30 signaling on B cell development and differentiation. In mice with B cell–specific CD30 expression, young animals displayed a normal phenotype, whereas aged mice developed pronounced expansions of B, T, and myeloid cells in the spleen, along with elevated frequencies of GC B cells and IgG1-switched cells. This expansion may be driven by CD4 + senescence-associated T cells and T follicular helper cells, which partly express CD30L (CD153) and may stimulate CD30 + B cells. Induction of CD30 in antigen-activated B cells accelerates GC reactions, enhances plasma cell differentiation – potentially via CXCR4 upregulation – and promotes accumulation of IgG1-switched cells with GC- or memory-like features. Collectively, these findings highlight the role of CD30 signaling in dysregulated lymphocyte activation and proliferation. Building on this, recent data suggest that CD30 signaling may also modulate B cell infiltration and differentiation within the lung, a process highly relevant to the pathogenesis of chronic obstructive pulmonary disease (COPD), where chronic B cell activation is a key driver of iBALT formation and disease pathogenesis. Publication History Article published online: 04 March 2026 © 2026. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany