The adhesive interactions of cells with other cells and with the extracellular matrix are crucial to all developmental processes, but have a central role in the functions of the immune system throughout life Three families of cell-surface molecules regulate the migration of lymphocytes and the interactions of activated cells during immune responses

Adhesion receptors of the immune system.

https://www.cell.com/cell/pdf/0092-8674(88)90434-5.pdf

Primary structure of ICAM-1 demonstrates interaction between members of the immunoglobulin and integrin supergene families

A cell adhesion molecule, ICAM-1, is the major surface receptor for rhinoviruses.

Cell communication is essential to development, tissue organization and function of all multicellular organisms. Cells communicate with each other and with their environment via soluble mediators and during direct contact. In the immune system leukocytes are involved in a host of cell-soluble mediator, cell-cell and cell-matrix interactions. For instance, an acute inflammatory response is initiated by release of soluble substances at the site of injury that direct leukocyte migration and localization. The circulating leukocytes arriving at the site of injury must directly adhere to the endothelium and basement membrane during extravasation from the circulation. Once in the tissue, leukocytes will migrate in response to gradients of chemoattractants and to adhesive gradients. The leukocytes will adhere and de-adhere to a variety of cells, finally find infected or antigen-presenting cells, adhere to them and deliver the appropriate immunological response. Discovery of several cell surface receptors involved in cell-cell, cell-substrate, or cell-soluble ligand binding has been a key factor in understanding the mechanisms underlying inflammatory and immune phenomena. Three protein families, the immunoglobulin (Ig) family (Williams & Barclay 1988, Williams 1987), the integrin family (Springer 1990, Kishimoto et al. 1989a, Hynes 1987, Ruoslahti & Pierschbacher 1987, Hemler 1988), and the recently designated selectin family (Tedder et al. 1989, Stoolman 1989, Springer 1990), have been described that are extensively involved in a network of cell-cell and cell-matrix interactions in the immune system. Engagement of these surface receptors can transduce a signal leading to cellular events that change the phenotype, movement, gene expression, or activation state of the cell. On the other hand, cytoplasmic signals regulate the functional activity and surface expression of these receptors. These receptors thus mediate a dialogue, transferring information in

Structure and function of leukocyte integrins.

Antisense oligonucleotides inhibit intercellular adhesion molecule 1 expression by two distinct mechanisms.

Although intercellular adhesion molecule-1 (ICAM-1) has been implicated as a ligand in some LFA-1-dependent adhesion, its importance to T cell function has not been established. The present studies investigate the importance of ICAM-1 for human cytotoxic T lymphocytes (CTL), both in their formation of antigen-independent conjugates (AIC) and in their lysis of targets. Analysis of monoclonal antibody (mAb) inhibition of AIC formation indicate that ICAM-1 mAb 1 blocks (a) AIC formation with some but not all targets; (b) the LFA-1 pathway but not the CD2/LFA-3 pathway of adhesion; (c) by binding to the target cell, not the T cell. In studies of cell-mediated lysis (CML) ICAM-1 mAb inhibited lysis of some targets, such as U-937, that use ICAM-1 predominantly in AIC formation; CML on some other targets is not inhibited by ICAM-1 mAb. These data indicate that ICAM-1 is a ligand for AIC formation, antigen-specific CTL recognition and cytolysis of particular target cells. The data also indicate that ICAM-1 is not used in LFA-1-dependent CTL interactions with all kinds of target cells, suggesting the existence of alternative ligands for LFA-1.

Functional evidence that intercellular adhesion molecule-1 (ICAM-1) is a ligand for LFA-1-dependent adhesion in T cell-mediated cytotoxicity.

Human T cell rosetting is mediated by LFA-3 on autologous erythrocytes.

Recent studies have shown that cytotoxic T lymphocytes form conjugates with antigen-negative targets.' These studies have further demonstrated that this process of antigen-independent conjugate formation (AIC) is mediated by way of two adhesion pathways: one involving the T cell-CD2 receptor binding to the ligand LFA-3* on the target, and the other involving the T cell-LFA-I receptor interacting with ICAM-1 and probably other ligandsj on the target. While the roles of CD2, LFA-I , and LFA-3 in CTL-mediated lysis (CML) have been demonstrated a b ~ n d a n t l y , ~ very little is known about the role of ICAM-I in such lysis. ICAM-I was initially proposed as a ligand for LFA-I , based upon monoclonal antibody (mAb) inhibition of LFA-1-dependent T-cell adhesion to fibroblasts and the finding that inhibition occurred with pretreatment of the fibroblasts and not the T cell.5.h These findings have been extended to and confirmed in AIC using CTL c1ones.j We initially investigated the role of ICAM-I by mAb-inhibition studies of AIC formation, and showed that its utilization in LFAI-dependent conjugates varied significantly between target^,^ irrespective of the ICAM1 level expressed on the target. To analyze its role in CML, targets that predominantly used ICAM-I in AIC were selected. One such target is U937 (a prornonocytic line).3 The ability of the ICAM-1 mAb to inhibit antigen-independent, phorbol myristic acetate (PMA)/ ionophore-triggered lysis of U937 by a CTL clone was studied. The results in FIGURE 1A showed that ICAM-1 mAb inhibits lysis by 70%; lysis is also inhibited well by the LFA-1 mAb (go%), and to a limited extent by CD2 (27%) and LFA-3 (38%) mAb. Following this result, a bulk population of allospecific T cells were prepared by two cycles of in vitro stimulation of peripheral blood mononuclear leukocytes with irradiated U937 as stimulator cells. The bulk population was tested in a standard C M L assay. The result in FIGURE 1B showed 75% inhibition by the ICAM-1 mAb, compared with 95%, 2096, and 15% inhibition by LFA-I , CD2, and LFA-3 mAb, respectively. These results showed that ICAM-I is critical for antigen-specific C T L recognition in this effectoritarget combination. Studies with various effectoritarget combinations revealed differing utilization and requirements for ICAM-1 in C T L r e ~ o g n i t i o n . ~ The results are consistent with the interpretation that ICAM-I can serve as one ligand for LFA-I in CTL recognition. The role of ICAM-1 in CTL recognition correlates closely with its ability to inhibit

Intercellular Adhesion Molecule‐1 (ICAM‐1) Monoclonal Antibody Inhibits Cytotoxic T Lymphocyte Recognition

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Functional evidence that intercellular adhesion molecule-1 (ICAM-1) is a ligand for LFA-1-dependent adhesion in T cell-mediated cytotoxicity.

Human T cell rosetting is mediated by LFA-3 on autologous erythrocytes.

Intercellular Adhesion Molecule‐1 (ICAM‐1) Monoclonal Antibody Inhibits Cytotoxic T Lymphocyte Recognition