Lymphocytes express specific antigen-independent contact interaction sites upon activation.

Cell contact between lymphocytes can be observed in the form of clustering in autologous cultures of rat or mouse lymph node cells. Mutual binding takes place in the absence of adherent cells and is displayed by B cells as well as by T cells, with the exception of immature (Lyt 1,2+) T cells. Contact formation is related to activation of the lymphocytes since thymidine-incorporating cells as well as plaque-forming cells are concentrated in the cluster cell fraction and the formation of clusters is greatly increased by periodate stimulation. The interaction is selective with respect to cell type (cells of other tissue origin are not bound) and differentiation (only activated lymphocytes and some of several lymphoid cell lines are able to interact). The reaction is not genetically restricted, but takes place even between different (but related) species. Neither antigen nor MHC structures are involved in contact formation. Protease treatment abolishes the ability to form clusters, but one part of the interacting receptor/acceptor structures is apparently trypsin resistant. The interaction is dependent on the presence of magnesium, whereas calcium ions have no supporting effect. Involvement of the cytoskeleton is shown by a partial inhibition of the cluster formation by cytochalasin B and azide. No indication for a lectin nature of the binding structures could be found by carbohydrate inhibition studies. The relation of this interaction mechanism to other models of physical interaction in the immune system as well as its possible function for signal exchange and local recruitment of activated cells is discussed.