Immunohistological detection of gap junctions in human lymphoid tissue: connexin43 in follicular dendritic and lymphoendothelial cells.

We investigated the expression of gap junction connexins26, -32, and -43 in normal,reactive, and diseased human lymphoid tissue with single and double immunolabelingand confocal laser scanning microscopy. In all tissues, connexin43 positivity wasdetected in follicular dendritic cells positive for CD21 and CD35 antigens, aroundlymphoendothelial cells moderately positive for Factor VIII, CD31 and cathepsin-Dantigens; and somewhat in vascular endothelia including high endothelial venulesstrongly positive for Factor VIII and CD31 antigens. The ultrastructural hallmark ofgap junctions, pentalaminar structures with appropriate spacing, was found infollicular dendritic cell processes. Connexin43 was also detected between smoothmuscle and stromal cells of the gut, in capsular fibroblasts, and in tonsilepithelium. Neither connexin32 nor -26 was revealed, except for connexin26 in thetonsil epithelium. In follicular dendritic cells, connexin43 co-localized closelywith the desmosomal proteins desmoplakin and desmoglein, suggesting that celladherence has a role in gap junction formation. Most connexin43 was observed in sinuslining cells of lymph nodes involved in malignancies and in follicular dendriticcells in the light zone of germinal centers where maturing but still proliferatinglymphocytes are situated. In the light of their distribution, gap junctions may playa part in regulating the growth of germinal centers and in integrating activating orcontrolling signals in follicular dendritic and sinus lining cell networks. Becauseconnexin43 is the connexin of stromal cells, finding it in follicular dendritic cellsin consistent with the proposal that these cells originate from resident stromalcells.