ELAM-1 is an adhesion molecule for skin-homing T cells

Picker, Louis J.; Kishimoto, Takashi; Smith, C. W.; Warnock, R A; Butcher, Eugene C.

doi:10.1038/349796a0

Cited by 779 publications

(373 citation statements)

References 21 publications

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“…In support of this idea, memory T cells expressing an E-selectin ligand, designated cutaneous lymphocyte Ag-1 (CLA-1), are enriched within inflamed dermis compared with peripheral blood. It has been proposed that CLA-1 ϩ memory T cells use persistent E-selectin on dermal EC as an address signal for skin homing (4).…”

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confidence: 99%

Cutting Edge: Internalization of Transduced E-Selectin by Cultured Human Endothelial Cells: Comparison of Dermal Microvascular and Umbilical Vein Cells and Identification of a Phosphoserine-Type Di-leucine Motif

Kluger

Shiao

Bothwell

et al. 2002

The Journal of Immunology

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Persistent E-selectin expression on human dermal microvascular endothelial cells (HDMEC), believed to mediate skin-specific T cell homing, results from a slow rate of surface protein internalization after cytokine induction. Following transduction of unactivated HDMEC with E-selectin cDNA, the rate of internalization was largely independent of increasing levels of surface protein expression, leading to prolonged t1/2 values of over 4 h, comparable to that observed following cytokine induction. In HUVEC, the rate of internalization increased with surface expression level, leading to an essentially constant t1/2 of under 2 h. Thus, the internalization process rather than cytokine responsiveness or E-selectin structure underlies the difference in endothelial cell behavior. Mutational analysis of the cytoplasmic region demonstrated a role for a di-leucine-type motif involving I588 and L589 but not for a putative tyrosine-type motif. Control of E-selectin surface expression appears to be phosphoserine dependent, since alanine but not aspartic acid substitution for S581 slows E-selectin internalization.

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confidence: 99%

Cutting Edge: Internalization of Transduced E-Selectin by Cultured Human Endothelial Cells: Comparison of Dermal Microvascular and Umbilical Vein Cells and Identification of a Phosphoserine-Type Di-leucine Motif

Kluger

Shiao

Bothwell

et al. 2002

The Journal of Immunology

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“…Parenthetically, IL-I and TNF-o can also be synthesized by thyroid epithelial cells [30,31 ]. E-selectin is not only involved in the adhesion of neutrophils and monocytes to EC in acute inflammation, but also plays an important role in the initial tethering of memory T cells to inflamed sites, as has been reported in chronic inflammation of the skin [32]. as well as in rheumatoid arthritis [13].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, Eselcctin binds to the glycosylated cutaneous lymphoid antigen (CLA, HECA-452 antigen) expressed by T and B eells [10], and P-selectin also recognizes the non-sialylated Lewis^ (Le^, CD15) [II]. E-and P-seleetins can interact not only with neutrophils and natural killer (NK) cells, but also with certain minor T cell subsets, chronically activated T cells, at those infilirating chronic inflammatory sites [12,13]. In addition, we have recently reported in HT the presence of sLe".…”

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confidence: 99%

Expression of vascular adhesion molecules on human endothelia in autoimmune thyroid disorders

Marazuela

Sánchez‐Madrid

Acevedo

et al. 1995

Clinical and Experimental Immunology

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SUMMARYCellular activation and expression of certain adhesion molecules within vascular endothelium is a critical event in leucocyte recruitment and emigration. A wide array of different adhesion receptors has been identified to mediate the interaction between endothelial cells (EC) and leucocyte subpopulations. In this study, the tissue expression of E-selectin. P-selectin. CD31. and endogiin endothelial cell adhesion molecules was studied on thyroid tissue from patients with Graves' disease (GD) and Hashimoto's thyroiditis (HT), We found an up-regulated expression of E-selectin in EC in GD and HT thyroids, specifically in those areas more severely inflamed, with no reactivity in control thyroids. P-selectin was basally expressed in postcapillary venules in control glands, wiih an increased expression in HT and GD glands. On the other hand, increased CD31 expression was found on perifollicular. small and large venule EC from GD and HT glands, that correlated with the severity of mononuclear infiltration. In addition. CD3I expression was observed in some intrathyroidai macrophages and T cells in close proximity to CD31^ EC. Furthermore, a markedly enhanced expression of endogiin, a transforming growth factor-beta binding protein, was mainly located on perifollicular EC and EC from small venules as well as In adjacent macrophages from GD and HT thyroid glands. This enhanced expresion of E-and P-selectins, CD31 and endogiin by thyroid EC in GD and HT may refiect their ability to regulate leucocyte trafficking and activation.

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“…These findings suggested that allergic response induced by IgE and mast cells causes preparation for infiltration of lymphocytes, eosinophils, and neutrophils into the bronchial mucosa. In other organs, e.g., intestine, skin, and lymph nodes, tissue-specific adhesion molecules, chemokines, and their receptors that recruit T cells have already been discovered (15)(16)(17)(18)(19). Despite these discoveries, it is not well known how T cells recirculate into the bronchial mucosa in allergic diseases such as asthma.…”

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confidence: 99%

T Cells of Atopic Asthmatics Preferentially Infiltrate Into Human Bronchial Xenografts in SCID Mice

Tsumori

Kohrogi

Goto

et al. 2003

The Journal of Immunology

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T cells play an important role in the pathogenesis of bronchial asthma. However, it is not completely known how circulating lymphocytes infiltrate into the airways of asthmatic patients. Because SCID mice are unable to reject xenogenic transplants, many xenotransplant models using various human tissues have been developed. Therefore, to examine the interaction between bronchi and T lymphocytes of asthma, it may be possible to use the human bronchial xenograft and PBMC xenograft in SCID mice. We transplanted human bronchi into the subcutaneum of SCID mice and i.p. injected PBMCs that were obtained from patients with atopic asthma, atopic dermatitis and rheumatoid arthritis, and normal subjects (asthmatic, dermatitis, rheumatic, and normal huPBMC-SCID mice). There was no difference in the percentage of CD3-, CD4-, CD8-, CD25-, CD45RO-, CD103-, and cutaneous lymphocyte Ag-positive cells in PBMCs among the patients with asthma, dermatitis, rheumatoid arthritis, and normal subjects, and CD3-positive cells in peripheral blood of asthmatic, dermatitis, rheumatic, and normal huPBMC-SCID mice. The number of CD3-, CD4-, and CD8-positive cells in the xenografts of asthmatic huPBMC-SCID mice was higher than those of dermatitis, rheumatic, and normal huPBMC-SCID mice. IL-4 mRNA and IL-5 mRNA were significantly higher in the xenografts of asthmatic huPBMC-SCID mice than those in the xenografts of normal huPBMC-SCID mice, but there were no significant differences in the expressions of IL-2 mRNA or IFN-γ mRNA between them. These findings suggest that T cells, especially Th2-type T cells, of asthmatics preferentially infiltrate into the human bronchi.

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ELAM-1 is an adhesion molecule for skin-homing T cells

Cited by 779 publications

References 21 publications

Cutting Edge: Internalization of Transduced E-Selectin by Cultured Human Endothelial Cells: Comparison of Dermal Microvascular and Umbilical Vein Cells and Identification of a Phosphoserine-Type Di-leucine Motif

Cutting Edge: Internalization of Transduced E-Selectin by Cultured Human Endothelial Cells: Comparison of Dermal Microvascular and Umbilical Vein Cells and Identification of a Phosphoserine-Type Di-leucine Motif

Expression of vascular adhesion molecules on human endothelia in autoimmune thyroid disorders

T Cells of Atopic Asthmatics Preferentially Infiltrate Into Human Bronchial Xenografts in SCID Mice

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