Photo Credit: nopparit
The following is a summary of “IL-25 Enhances B Cell Responses in Type 2 Inflammation Through IL-17RB Receptor,” published in the January 2025 issue of Allergy and Immunology by Abdu et al.
IL-25 promotes type 2 inflammation in asthma and chronic rhinosinusitis with nasal polyps (CRSwNP), targeting ILC2 and Th2 cells. Other cellular targets for IL-25 are not well defined.
Researchers conducted a retrospective study on IL-25 receptor (IL-17RB) expression in B cells and their response to IL-25 in vitro.
They evaluated IL-17RB expression, regulation, and function in peripheral blood-derived B cells using flow cytometry and RT-PCR, including in response to IgE-inducing stimuli (anti-CD40 mAb and IL-4). Single-cell RNA sequencing compared IL-17RB+ and IL-17RB- B cells. They also compared B cell IL-17RB expression in type 2 inflamed tissue, using B cells from nasal polyps, control turbinate tissue, and matched peripheral blood.
The results showed that activation of B cells with anti-CD40 and IL-4 increased IL-17RB expression at both protein and mRNA levels, further upregulated by IL-25. IL-17RB+ B cells responded to IL-25 with enhanced antibody production. Single-cell RNA-sequencing revealed higher expression of IGHE, CCL17, and CCL22 in IL-17RB+ B cells compared to IL-17RB- B cells. B cells from nasal polyp tissue expressed higher surface IL-17RB than control tissue, correlating with CRSwNP severity (SNOT-22).
Investigators concluded that IL-17RB+ B cells, with a distinct transcriptional profile, enhanced antibody production in response to IL-25. This highlighted the IL-25/IL-17RB pathway as a potential therapeutic target for CRSwNP and other type 2 inflammatory disorders.
Source: onlinelibrary.wiley.com/doi/full/10.1111/all.16472
