Abstract
The investigation of cell-substrate adhesion structures and cell-cell interaction molecules may be crucial to understanding the traffic and distribution of malignant lymphoid cells. In this Vespect, B-chronic lymphocytic leukemia (B-CLL) is a useful model because of three reasons. First, malignant B-CLL cells relentlessly accumulate in lymphoid organs and the bone marrow, but fail, in large part, to recirculate (1), suggesting the existence of adhesion abnormalities. Second, the cytoskeletal organization of B-CLL cells differs from that of normal B lymphocytes (2). B-CLL cells adhere spontaneously in vitro utilizing, instead of the conventional “adhesion plaques”, dot-shaped close contact sites similar to the podosomes described in cells of monocyte-macrophage lineage and in class I oncogene-transformed cells (3–5). Third, the cytoskeleton function of B-CLL cells may be abnormal as suggested by the observation that different ligands, including surface immunoglobulins (slg), are capped sluggishly if at all (6,7).KeywordsFollicular LymphomaAlpha ChainBeta2 IntegrinAdhesion PlaqueCell BioIThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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