The Role of the LFA‐1/ICAM‐1 Interaction in Human Leukocyte Homing and Adhesion

Wawryk, SO; Novotný, J; Wicks, Ian P.; Wilkinson, David; Maher, Darryl; Salvaris, Evelyn; Welch, Karen; Fecondo, John V.; Boyd, Andrew W.

doi:10.1111/j.1600-065x.1989.tb00016.x

Cited by 242 publications

(79 citation statements)

References 61 publications

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“…ICAM-1 is widely distributed on both lymphoid and non-lymphoid cells and is constitutively expressed on vascular endothelial cells, tonsillar mucosal epithelial cells, and activated T-and B-lymphocytes. It has an overall distribution similar to that of the major histocompatibility complex (MHC) molecule, human-leukocyteassociated antigen (HLA)-DR (Wawryck et al, 1989). ICAM-1 is markedly up-regulated by a variety of inflammatory stimuli, such as tumor necrosis factor and interleukin 1 (Dustin et al, 1986), and it appears that this up-regulation is important in the adhesion and migration of circulating neutrophils and monocytes which bind ICAM -1 via their P2 integrin.…”

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Cell Adhesion Molecules and Oral Cancer

Thomas

Speight

2001

Critical Reviews in Oral Biology & Medicine

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Cell adhesion molecules (CAMs) are found on the surfaces of all cells, where they bind to extracellular matrix molecules or to receptors on other cells. As well as having a structural role, CAMs function as signaling receptors, transducing signals initiated by cellular interactions which regulate many diverse processes, including cell division, migration, and differentiation. Cell adhesion molecules are essential for maintaining stable tissue structure. However, cell adhesion must be dynamic to facilitate the mobility and turnover of cells. In dynamic situations, cells alter their cell-cell and cell-matrix interactions by virtue of altered expression and function of CAMs. The expression of CAMs is normally tightly regulated, thereby controlling cell proliferation, mobility, differentiation, and survival. Many of these processes are misregulated in malignant tumors, and it has been shown that many of the characteristics of tumor cells are attributable to the aberrant expression or function of CAMs.Integrins and E-cadherin are the most important CAMs expressed by stratified squamous epithelium. Altered expression of these molecules has been found in oral carcinoma, where loss of CAM expression is often seen in poorly differentiated lesions.However, up-regulation of certain integrins, such as av16, has consistently been found in oral cancer, suggesting that it may play an active role in disease progression.Key words. Oral cancer, cell adhesion molecules, integrins, cadherins, selectins, immunoglobulin superfamily, CD44. (I) IntroductionCell adhesion molecules (CAMs) are found on the surfaces of all cells, where they bind to extracellular matrix molecules or to receptors on other cells. Cell adhesion is critical in the dynamic processes necessary for tissue morphogenesis in development and the maintenance of complex differentiated tissues in adult organisms. CAMs serve in these roles by virtue of their capacity to connect the exterior of the cell with the interior. They form structural linkages between the cell cytoskeleton and the extracellular matrix or between cells, and also function as signaling receptors, transducing signals initiated by cellular interactions which regulate many diverse processes, including cell division, migration, and differentiation ( Fig. 1).Cell adhesion molecules are essential for maintaining the stable structure of stratified squamous epithelium. In normal epithelium, keratinocytes are attached to each other and to the underlying basement membrane. Cell adhesion, however, must be dynamic to facilitate the mobility and turnover of cells. In dynamic situations, keratinocytes alter their cell-cell and cell-ECM interactions by virtue of altered expression and function of CAMs.The expression of cell adhesion molecules is normally tightly regulated-forming, persisting, or declining in an ordered fashion. This allows for controlled cell proliferation, mobility, differentiation, and survival. Many of these processes are misregulated in malignant tumors, and it has been shown that man...

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Cell Adhesion Molecules and Oral Cancer

Thomas

Speight

2001

Critical Reviews in Oral Biology & Medicine

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“…Also expressed are the cell surface molecules: Thy-1, CD2, CD16, CD44, heat stable antigen (HSA), thymic shared antigen (TSA-1), CD18 (LFA-1), CD54 (ICAM-1), Ly-6, CD26 (THAM-1) and the cx chain of the II.-2 receptor (CD25) (10)(11)(12)(13)(14)(15)(16)(17). Markers such as CD25, ICAM-1, CD44, and Ly-6 are prominent on mature T lymphocytes only after TCR activation (15,18,19). Thus, some aspects of the activation program that are triggered in mature T cells by TCR engagement are found in T cell progenitors in the absence of TCR signaling.…”

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Gene transcription in differentiating immature T cell receptor(neg) thymocytes resembles antigen-activated mature T cells.

Zúñiga‐Pflücker

Schwartz

Lenardo

1993

The Journal of Experimental Medicine

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SummaryEarly in ontogeny thymocytes have a surface marker phenotype that resembles activated mature T cells but they lack expression of the T cell receptor (TCR) complex. We have made preparations of day 14/15 triple negative fetal thymocytes that exhibit the activated T lymphocyte markers CD25, intercdlular adhesion molecule 1, Ly-6A/E, CD44, and heat stable antigen and are rapidly proliferating as evidenced by flow cytometric examination of BrdU incorporation. We found that binding activities of the gene regulators nuclear factor (NF)-gB, the NF-gB p50 homodimer complex, nuclear factor of activated T cells (NF-AT), oct-l, oct-2, activator protein 1 (AP-1), and serum response factor (SRF), are all present in these early thymocytes. Whereas the octamer factors and SRF persist during ontogeny, NF-gB, NF-AT, and AP-1 decrease and are undetectable in the adult thymus. Transfection of disaggregated thymocytes by dectroporation or intact thymic lobes by gold-particle bombardment revealed that reporter constructs for NF-gB, NF-AT, AP-1, octamer factors and, to a small extent, the TCR-ot enhancer were active in early thymocyte development. We rigorously diminated the possibility that these transcriptional events were due to minor populations of TCR + cells by showing that these reporter constructs were also active in recombinase activating gene (RAG) -/. thymocytes that are incapable of completing TCR gene rearrangement, and predominantly contain cells that have an activated phenotype. Thus, transcriptional events that are usually triggered by antigen stimulation in mature T cells take place early in thymic ontogeny in the absence of the TCR. Our analysis suggests that there are striking regulatory similarities but also important differences between the activation processes that take place in antigen-stimulated mature T cells and thymic progenitor cells.

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“…We have shown that anti-ICAM-1 blocks T-dependent B cell activation (8) and cytotoxic T-lymphocyte target recognition and activation (9,10), and inflammatory responses (4,11) are also inhibited. It was originally thought that LFA-1 and ICAM-1 acted solely as adhesion molecules, strengthening otherwise weak interactions between cells.…”

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“…It is a ligand for LFA-1 (CD11a/CD18), Mac-1 (CD11b/CD18), CD43, rhinovirus, and fibrinogen, and it participates in cellular interactions by binding to its several ligands via different domains. ICAM-1 is expressed constitutively at low levels on lymphocytes, vascular endothelium, and a variety of other cell types (3,4). In vivo, high levels are expressed on tissues involved in inflammatory responses (5,6).…”

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