The following is a summary of “Neutrophilic granulocyte-derived B-cell activating factor supports B cells in skin lesions in hidradenitis suppurativa,” published in the APRIL 2023 issue of Allergy (& Immunology) by Sabat, et al.
For a study, researchers sought to investigate the role of mediators that support the persistence of B/plasma cells in patients with Hidradenitis suppurativa (HS), a chronic inflammatory disease characterized by painful nodules, abscesses, and pus-draining tunnels in specific skin areas (axillary, inguinal, and perianal).
Researchers conducted mRNA sequencing, quantitative PCR on reverse-transcribed RNA, flow cytometry, and immunohistofluorescence analyses on skin samples obtained from various cohorts of HS patients and control groups. They also examined blood plasma, cultured skin biopsy samples, and different cell types such as keratinocytes, dermal fibroblasts, neutrophilic granulocytes (neutrophils), monocytes, and B cells. Complex systems biology approaches were used to analyze bulk and single-cell RNA sequencing data.
The study revealed elevated proportions of B/plasma cells, neutrophils, CD8+ T cells, M0 macrophages, and M1 macrophages in HS lesions compared to healthy skin and perilesional intertriginous areas. B/plasma cells, neutrophils, and B-cell activating factor (BAFF, also known as TNFSF13B) were found to be associated. BAFF was highly abundant in HS lesions, particularly in nodules and abscesses. The main producers of BAFF in HS lesions were myeloid cells. The secretion of BAFF by neutrophils was primarily stimulated by granulocyte colony-stimulating factors in the presence of bacterial products. Upregulation of BAFF receptors in HS lesions was observed in B cells (TNFRSF13C/BAFFR and TNFRSF13B/TACI) and plasma cells (TNFRSF17/BCMA). The characterization of the lesional BAFF pathway identified various molecules involved in B/plasma cell migration/adhesion (e.g., CXCR4, CD37, CD53, SELL), proliferation/survival (e.g., BST2), activation (e.g., KLF2, PRKCB), and reactive oxygen species production (e.g., NCF1, CYBC1).
The study findings suggested that neutrophil-derived BAFF plays a crucial role in supporting the persistence and function of B/plasma cells in HS lesions.