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Syn‐ capping of human T lymphocyte adhesion/activation molecules and their redistribution during interaction with endothelial cells
Author(s) -
Rosenman Stephen J.,
Ganji Amir A.,
Tedder Thomas F.,
Gallatin W. Michael
Publication year - 1993
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.53.1.1
Subject(s) - microbiology and biotechnology , biology , cell adhesion molecule , pseudopodia , cell adhesion , lymphocyte , lymphocyte function associated antigen 1 , cell , cell–cell interaction , intercellular adhesion molecule 1 , biophysics , immunology , actin , biochemistry
Lymphocyte‐endothelial cell interactions are mediated in part by multiple lymphocyte surface adhesion/activation molecules and their cognate ligands. We investigated the surface localization of several of these molecules implicated in T cell adhesion and transen‐ dothelial migration mechanisms to determine if spatial regulation of their distribution contributes to these processes. T lymphocyte suspensions were stained to define distribution, ability to be aggregated into energy‐ dependent caps, and potential cocapping of several adhesion structures. CD2, CD44, L‐selectin (LAM‐1, LECCAM‐1), and CDlla/CD18 (LFA‐1) exhibited uniform distribution on the T cell surface by direct immunofluorescence but formed caps in an energy‐ dependent, and therefore cytoskeletally driven, manner when examined by indirect immunofluorescence. CD2 was shown to syn‐cap (unidirectionally cocap) with GD44 and CDlla/CD18 (LFA‐1), an observation potentially related to functional cooperation among these molecules in T cell activation. T cells were also added to endothelial cell monolayers to assess, in a physiologically relevant context, potential surface molecule reorganization. Lymphocytes co‐cultured with human umbilical vein endothelial cells (HUVEC) underwent a profound shape change, from essentially round cells to polarized cells bearing pseudopodia. Immunofluorescent localization of T cell adhesion/activation molecules using confocal microscopy revealed the redistribution of CD2, CD44, and L‐selectin to the pseudopod. In contrast, CDlla/CD18 remained globally distributed on the cell surface, even in severely deformed cells. Both lymphocyte shape change and membrane molecule redistribution appear to be cell‐cell contact‐dependent phenomena requiring intact, viable endothelial cells. Mechanisms that control these events may be critical to lymphocyte recirculation and inflammation.