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In their article in this issue of The Journal , Ping, et al used in vitro cultures of epithelial cells from salivary gland tissues of patients with Sjogren’s syndrome (SS), and from control patients lacking inflammatory infiltrates1.The basic process of salivary gland cell death (apoptosis) was similar both in SS salivary epithelial cells and in normal salivary epithelial cells. Thus, the key difference in the salivary gland dysfunction of the patient with SS in vivo appears to be the presence of focal T cell infiltrate in the SS gland that serves as a source of CD40 ligand (CD40L).Although their article is a nice exercise in molecular biology, with the expected molecular gymnastics (electrophoretic mobility shifts, Western blots, and TUNEL assays), the ultimate questions that arise are: What do these results mean for the patient with SS with dry mouth? How do these results influence the future for therapeutic selection of options?The current study by Ping, et al is an extension of their report from 2005 on the role of CD40 and Fas in SS salivary gland cells2. Subtle points in the present study include the observation that inhibition of p38 and nuclear factor-κB (NF-κB) activation does not fully prevent CD95-mediated apoptosis (see their Figure 4). So there must be other pathways that CD40 is activating.Particularly in the regulation of p38 and NF-κB, many different factors influence their canonical and noncanonical activation. Thus, additional factors in situ determine the … Address correspondence to Dr. Fox. E-mail: robertfoxmd{at}mac.com

The Salivary Gland Epithelial Cell in Sjögren’s Syndrome: What Are the Steps Involved in Wounding or Killing Their Secretory Function?