Expression of the cutaneous lymphocyte antigen and the αIELβ7 integrin by intraepithelial lymphocytes in healthy and diseased human gingiva

Tonetti, Maurizio S.; Straub, Antje M.; Lang, Niklaus P.

doi:10.1016/0003-9969(95)00084-4

Cited by 18 publications

(15 citation statements)

References 31 publications

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“…Recent evidence from immunocytochemical studies of diseased skin suggests expression of αeβ7 by IEL correlates with epidermotropism 16 and large numbers of αeβ7‐positive IEL are found in inflamed gingiva and in the buccal mucosa in oral lichen planus 14 ,. 36 It may be that interaction of αeβ7 with the unknown ligand on keratinocytes is a more important adhesion mechanism than LFA‐1/ICAM‐1 interaction.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of binding of cutaneous lymphocyte‐associated antigen‐positive and αeβ7‐positive lymphocytes to oral and skin keratinocytes

Brown¹,

Furness

Speight

et al. 1999

Immunology

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Intraepithelial lymphocytes (IEL) utilize the integrin alphaebeta7 on their surface to bind to E-cadherin on epithelial cells in the gut and breast. In oral mucosa and skin IEL express alphaebeta7 and the cutaneous lymphocyte-associated antigen (CLA) but the mechanisms of adhesion of these subsets to keratinocytes are unknown. Levels of alphaebeta7 and CLA were up-regulated on peripheral blood lymphocytes (PBL) by transforming growth factor-beta (TGF-beta) and interleukin-12 (IL-12), respectively, and both groups of lymphocytes adhered onto oral and skin keratinocytes. Adhesion of IL-12-activated PBL was totally abolished by anti-lymphocyte-associated function antigen type 1 (anti-LFA-1) antibodies but was unaffected by anti-alphaebeta7 antibodies indicating that adhesion of the CLA-positive subset is mediated via LFA-1 interaction with intercellular adhesion molecule-1 (ICAM-1). Adhesion of TGF-beta-activated PBL to E-cadherin-positive oral and skin keratinocytes was partially inhibited by anti-alphaebeta7 antibodies but was unaffected by the blocking antibody E4.6 against E-cadherin which detects the binding site for alphaebeta7-positive lymphocytes in breast and gut epithelium. TGF-beta-activated PBL also bound to an E-cadherin-negative oral keratinocyte cell line and adhesion was inhibited by anti-alphaebeta7 antibodies. These results strongly suggest that in oral epithelium and epidermis alphaebeta7-positive lymphocytes do not bind to E-cadherin and there may be a novel second ligand for the alphaebeta7 integrin.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of binding of cutaneous lymphocyte‐associated antigen‐positive and αeβ7‐positive lymphocytes to oral and skin keratinocytes

Brown¹,

Furness

Speight

et al. 1999

Immunology

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“…These migrating leukocytes are present in health but dramatically increase in number with the accumulation of dental plaque and are closely associated with the development of gingival inflammation. Lymphocytes (particularly T lymphocytes) are also found with an intraepithelial distribution in the junctional epithelium (225).…”

Section: Structure and Compositionmentioning

confidence: 99%

Molecular and cell biology of the gingiva

Bartold¹,

Walsh²,

Narayanan³

2000

Periodontology 2000

187

151

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“…SLe x and sLe a oligosaccharides serve as crucial decorations on ligands for E-selectin and play signi®cant roles in haematogenous metastasis of cancer. However the tumour in the primary and metastatic lesions has a heterogeneous expression of sLe xrelated antigens (Tonetti et al 1995). It has been shown that endothelial cells adjacent to the metastatic lesion express E-selectin more extensively than those adjacent to primary foci.…”

Section: Discussionmentioning

confidence: 99%