CD4+ T lymphocyte subsets express connexin 43 and establish gap junction channel communication with macrophages in vitro

• Published in: Journal of leukocyte biology Vol. 82; no. 3; pp. 608 - 612
• Main Authors: Bermudez-Fajardo, Alexandra, Ylihärsilä, Minna, Evans, W Howard, Newby, Andrew C, Oviedo-Orta, Ernesto
• Format: Journal Article
• Language: English
• Published: United States Society for Leukocyte Biology 01.09.2007
• Subjects: Animals; CD4 Antigens - metabolism; CD4-Positive T-Lymphocytes - metabolism; Cell Communication - physiology; Connexin 43 - genetics; Connexin 43 - metabolism; Cytokines - metabolism; Flow Cytometry; Gap Junctions - metabolism; Immune System - physiology; inflammation; intercellular; Ion Channels - physiology; Lipopolysaccharides - pharmacology; lymphocytes; Macrophages - metabolism; Male; Mice; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - genetics; RNA, Messenger - metabolism
• ISSN: 0741-5400; 1938-3673
• DOI: 10.1189/jlb.0307134

Gap junction channels constructed of connexins (Cxs) are expressed by peripheral and secondary lymphoid organ‐derived lymphocytes. These channels in the plasma membrane play key roles in a range of lymphocyte functions exemplified by the synthesis and secretion of Igs and cytokines and during transmigration across the endothelium. Most recently, their involvement in antigen cross‐presentation has also been established. We report here for the first time the expression of mRNA and protein encoding Cx43 in mouse‐derived CD4+ Th0, Th1, and Th2 lymphocyte subpopulations and demonstrate the establishment gap junction channel formation with primary macrophages in vitro. We show that this mode of direct communication is particularly favored in Th1‐macrophage interactions and that LPS inhibits lymphocyte‐macrophage cross‐talk independently of the subset of lymphocyte involved. Our work suggests that gap junction‐mediated communication can be modulated in the absence of specific antigenic stimulation. Therefore, a further mechanism featuring gap junction‐mediated communication may be implicated in immune regulation.