Leukocyte-endothelial cell recognition: Three (or more) steps to specificity and diversity

Butcher, Eugene C.

doi:10.1016/0092-8674(91)90279-8

Cited by 2,646 publications

(1,549 citation statements)

References 20 publications

Supporting

Mentioning

1,505

Contrasting

Unclassified

Order By: Relevance

“…VCAM1 is a transmembrane endothelial glycoprotein, which plays a critical role during inflammatory reaction by permitting the recruitment of leukocytes at the inflammatory sites. It contributes to the rolling and adhesion of leukocytes during the process of leukocyte diapedesis via high-affinity binding to its counter receptor a4 1 expressed at the leukocyte cell surface 27,28 . Another contributor to VCAM1-mediated leukocyte diapedesis was identified as being SPARC 25 .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Tumour-derived SPARC drives vascular permeability and extravasation through endothelial VCAM1 signalling to promote metastasis

et al. 2015

View full text Add to dashboard Cite

Disruption of the endothelial barrier by tumour-derived secreted factors is a critical step in cancer cell extravasation and metastasis. Here, by comparative proteomic analysis of melanoma secretomes, we identify the matricellular protein SPARC as a novel tumour-derived vascular permeability factor. SPARC deficiency abrogates tumour-initiated permeability of lung capillaries and prevents extravasation, whereas SPARC overexpression enhances vascular leakiness, extravasation and lung metastasis. SPARC-induced paracellular permeability is dependent on the endothelial VCAM1 receptor and p38 MAPK signalling. Blocking VCAM1 impedes melanoma-induced endothelial permeability and extravasation. The clinical relevance of our findings is highlighted by high levels of SPARC detected in tumour from human pulmonary melanoma lesions. Our study establishes tumour-produced SPARC and VCAM1 as regulators of cancer extravasation, revealing a novel targetable interaction for prevention of metastasis.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Leukocyte engagement of VCAM1 on endothelial cells elicits multiple signalling pathways that participate to vascular function including paracellular permeability 27,28 . We therefore examined the impact of tumour-derived SPARC on endothelial cell signalling.…”

Section: Tumour-derived Sparc Induces Vascular Permeability In Vitromentioning

confidence: 99%

Tumour-derived SPARC drives vascular permeability and extravasation through endothelial VCAM1 signalling to promote metastasis

et al. 2015

View full text Add to dashboard Cite

show abstract

“…The initial process of`sampling' by neutrophils on the endothelial surface, seen as rolling, 12 occurs by a loose lectin±carbohydrate interaction involving selectins on the vessel wall and their ligand sialyl Lewis x expressed on neutrophils. Sulphated tetrasaccharide heparin fragments have been shown to compete with this ligand and reduce thioglycollate-induced in¯ammation in mice.…”

Section: Discussionmentioning

confidence: 99%

Treatment of corticosteroid‐resistant ulcerative colitis with heparin —a report of 16 cases

Evans

Wong

Morris

et al. 1997

Aliment Pharmacol Ther

135

View full text Add to dashboard Cite

Background:Heparin, a group of sulphated glycosaminoglycans, in addition to its anticoagulant activity, has a wide range of potentially anti‐inflammatory effects. These include inhibition of neutrophil elastase and inactivation of chemokines. Previous reports of fortuitous improvement in ulcerative colitis patients treated with heparin for prophylaxis of venous thrombosis, prompted us to perform a pilot study in patients with corticosteroid‐resistant ulcerative colitis.Methods:Sixteen hospitalized patients in relapse from ulcerative colitis and unresponsive to high‐dose corticosteroid therapy were treated with intravenous standard heparin (subcutaneous in two patients), the dose was adjusted to provide standard anticoagulant activity. Five patients continued with subcutaneous injections on discharge, with a gradual reduction in the frequency of doses.Results:Within 1 week of starting heparin, 12/16 patients had shown a considerable reduction in stool frequency. After 2 weeks of heparin therapy median stool frequency had improved from 8.0/day (range 6.3–10.0) pre‐treatment to 3.5/day (2.5–5.25) (P=0.008), and by 4 weeks 12/16 achieved clinical remission. Four patients required elective colectomy. Three patients were treated with heparin on a second occasion during a relapse, two failed to respond and required subsequent colectomy. Nine remain well. No serious complications were seen due to the anticoagulant activity, apart from bruising at subcutaneous injection sites.Conclusion:The response to heparin in patients with ulcerative colitis resistant to standard therapy is encouraging and supports the previous uncontrolled evidence for a therapeutic effect. A controlled trial of heparin in ulcerative colitis is clearly indicated.

show abstract

“…Before cultured TILs can migrate from the circulation into tissue they must first recognize and bind to tumour endothelium, a process determined by the adhesion molecules expressed on TILs and the presence of appropriate ligands on tumour endothelium (Butcher, 1991;Shimizu et al, 1992;Whiteside and Herberman, 1992). In the present study we determined the detailed phenotype of cultured TILs, with particular reference to the adhesion molecules they express, and assessed their ability to bind to endothelium in vitro.…”

Section: Tils Display Strong Activation-independent Binding To Endothmentioning

confidence: 99%

Adhesion of tumour-infiltrating lymphocytes to endothelium: a phenotypic and functional analysis

Adams

Yannelli²,

Newman³

et al. 1997

Br J Cancer

View full text Add to dashboard Cite

Summary Efficacy of cancer immunotherapy with cultured tumour-infiltrating lymphocytes (TlLs) depends upon infused TILs migrating into tumour-bearing tissue, in which they mediate an anti-tumour response. For TILs to enter a tumour, they must first bind to tumour endothelium, and this process depends on TILs expressing and regulating the function of relevant cell-surface receptors. We analysed the cell-surface phenotype and endothelial binding of TILs cultured from human melanoma and compared them with peripheral blood T cells and with allostimulated T cells cultured under similar conditions. Compared with peripheral blood T cells, TILs expressed high levels of five integrins, two other adhesion molecules, including the skin homing molecule CLA, and several activation markers and showed markedly enhanced integrin-mediated adhesion to a dermal microvascular endothelial cell line in vitro. Compared with the allostimulated T cells, TILs expressed higher levels of the cutaneous lymphocyte antigen (CLA), the adhesion molecule CD31 and the activation markers CD30 and CD69, but lower levels of several other adhesion and activation molecules. These phenotypic and functional properties of TILs should have complex effects on their migration in vivo. Expression of CLA, the skin homing receptor, may increase migration to melanoma (a skin cancer), whereas integrin activation may cause non-specific binding of TILs to other endothelium. Manipulation of the culture conditions in which TILs are expanded might result in a phenotype that is more conducive to selective tumour homing in vivo.

show abstract

Leukocyte-endothelial cell recognition: Three (or more) steps to specificity and diversity

Cited by 2,646 publications

References 20 publications

Tumour-derived SPARC drives vascular permeability and extravasation through endothelial VCAM1 signalling to promote metastasis

Tumour-derived SPARC drives vascular permeability and extravasation through endothelial VCAM1 signalling to promote metastasis

Treatment of corticosteroid‐resistant ulcerative colitis with heparin —a report of 16 cases

Adhesion of tumour-infiltrating lymphocytes to endothelium: a phenotypic and functional analysis

Contact Info

Product

Resources

About