Role of interaction between B cells and epithelial cells in pSS

We read with great interest the recent publication by Riviere et al , concerning the activation of B cells by salivary gland epithelial cells (SGECs) from patients with primary Sjogren’s syndrome (pSS).1 The authors elegantly show that coculture of CD19+ peripheral blood B cells with SGECs isolated from labial salivary glands (LSGs) of patients with pSS increases expression of the B cell activation marker CD38, and the memory B cell marker CD27. This effect was the most noticeable with further stimulation of toll-like receptor 3 by means of Poly(I:C) medium supplementation. Treatment of cocultures with agents ablating specific B cell signalling pathways (ibrutinib, blocking BTK signalling), and non-B cell specific pathways (LY294002 blocking the PI3K pathway and leflunomide, inhibiting lymphocyte proliferation) reduced this effect somewhat. We would like to take the opportunity to comment on these interesting findings. First, their main conclusion is that SGECs (by presumption ductal cells) from patients with pSS support the activation and survival of B cells. We would like to add that we have previously demonstrated in situ the presence of an epithelium-associated subset of B cells, expressing FcRL4, in both minor (labial) and major (parotid) SGs of patients with …

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