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EffectsCells: Expression and Proinflammatory CD40 on Adult Human Airway Epithelial

CD40/CD40 ligand interaction is an important pathway for B and T cell cooperation and function; functional CD40 molecules have recently been found on nonhematopoietic cells. We detected CD40 in vivo on normal human respiratory epithelial cells and showed that its expression is increased on inﬂamed airway epithelium. Subsequently, we analyzed its expression and function on primary cultures of human airway epithelial cells. Our data show that CD40 is up-regulated by IFN- (cid:1) and IFN- (cid:2) , its ligation increases the surface expression of CD54 and CD106 and it may stimulate the release of IL-6 and IL-8. The use of Janus kinase 3 (JAK3) and NF- (cid:3) B inhibitors suggests that both basal and CD40-induced release of the two cytokines is JAK3-dependent. Using colocalization techniques, we revealed the existence of CD40/JAK3 and CD40/TNFR-associated factor 2 interplay. The extent of these interactions may be partial (2–40% of the cells) or massive (80–90% of the cells) in cultured cells. Stimulation via CD40 causes a signiﬁcant increase in the number of cells expressing colocalization only in the cultures displaying low frequency of initial colocalization. Thus, airway epithelial cells, activated by CD40, may behave as effector cells of the inﬂammation process and should be considered priority targets for anti-inﬂammatory therapy. This work identiﬁes CD40 and the correlated JAK3 signaling molecule as potential molecular targets to block the inﬂammatory functions of epithelial cells. The Journal of Immunology, 2004, 172: 3205–3214.