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Titolo:
Inhibition by dexamethasone of Langerhans cell migration: influence of epidermal cytokine signals
Autore:
Cumberbatch, M; Dearman, RJ; Kimber, I;
Indirizzi:
Zeneca Cent Toxicol Lab, Macclesfield SK10 4TJ, Cheshire, England Zeneca Cent Toxicol Lab Macclesfield Cheshire England SK10 4TJ e, England
Titolo Testata:
IMMUNOPHARMACOLOGY
fascicolo: 3, volume: 41, anno: 1999,
pagine: 235 - 243
SICI:
0162-3109(199904)41:3<235:IBDOLC>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; DRAINING LYMPH-NODES; DENDRITIC CELLS; FACTOR-ALPHA; CONTACT SENSITIZATION; IMMUNE-RESPONSES; GENE-EXPRESSION; HUMAN-MONOCYTES; KAPPA-B; FLUORESCEIN ISOTHIOCYANATE;
Keywords:
dexamethasone; Langerhans cells; dendritic cells; tumour necrosis factor alpha; interleukin 1 beta;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Cumberbatch, M Zenecaandnt Toxicol Lab, Alderley Pk, Macclesfield SK10 4TJ, Cheshire, Engl Zeneca Cent Toxicol Lab Alderley Pk Macclesfield Cheshire England SK10 4TJ
Citazione:
M. Cumberbatch et al., "Inhibition by dexamethasone of Langerhans cell migration: influence of epidermal cytokine signals", IMMUNOPHARM, 41(3), 1999, pp. 235-243

Abstract

The influence of dexamethasone (DEX), a synthetic glucocorticoid, on the induction in mice of Langerhans cell (LC) migration has been investigated. Systemic treatment of mice with DEX was found to inhibit significantly the ability of a topically applied contact allergen (oxazolone) to induce the migration of LC from the epidermis and their subsequent accumulation as dendritic cells (DC) in draining lymph nodes. The stimulation of LC migration during skin sensitization is dependent upon signals provided by the epidermalcytokines tumour necrosis factor alpha (TNF-alpha) and interleukin 1 beta (IL-1 beta). It was found that treatment with DEX was unable to inhibit either LC migration or DC accumulation induced by the intradermal injection ofTNF-alpha. In contrast, LC migration provoked by similar exposure of mice to IL-1 beta (the action of which is dependent upon the de novo synthesis of TNF-alpha) was inhibited by DEX as was the arrival of DC in draining lymph nodes induced by this cytokine. Taken together, the data reported here indicate that DEX is able to inhibit very markedly the stimulation of LC migration during skin sensitization and it is proposed that such inhibition mayrepresent an important aspect of the immunosuppressive properties of glucocorticoids and of their proven utility in the treatment of cutaneous inflammatory disorders. The results also indicate that DEX does not inhibit LC migration secondary to direct effects on cell motility. The proposal is that impaired LC migration results from the regulation by DEX of the de novo synthesis and/or release of TNF-alpha an inducible epidermal cytokine that provides one important signal for LC to traffic from the skin. (C) 1999 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 04:43:38