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Titolo:
Interleukin (IL)-18 induces Langerhans cell migration by a tumour necrosisfactor-alpha- and IL-1 beta-dependent mechanism
Autore:
Cumberbatch, M; Dearman, RJ; Antonopoulos, C; Groves, RW; Kimber, I;
Indirizzi:
Syngenta Cent Toxicol Lab, Macclesfield SK10 4TJ, Cheshire, England Syngenta Cent Toxicol Lab Macclesfield Cheshire England SK10 4TJ England Univ Coll London, Ctr Dermatol, London WC1E 6BT, England Univ Coll LondonLondon England WC1E 6BT matol, London WC1E 6BT, England
Titolo Testata:
IMMUNOLOGY
fascicolo: 3, volume: 102, anno: 2001,
pagine: 323 - 330
SICI:
0019-2805(200103)102:3<323:I(ILCM>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
DRAINING LYMPH-NODES; HUMAN KERATINOCYTES; DENDRITIC CELLS; CONTACT SENSITIVITY; RECEPTOR; MICE; MURINE; IL-18; EXPRESSION; INDUCTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Cumberbatch, M Syngenta Cent Toxicol Lab, Alderley Pk, Macclesfield SK10 4TJ, Cheshire, England Syngenta Cent Toxicol Lab Alderley Pk Macclesfield Cheshire England SK10 4TJ
Citazione:
M. Cumberbatch et al., "Interleukin (IL)-18 induces Langerhans cell migration by a tumour necrosisfactor-alpha- and IL-1 beta-dependent mechanism", IMMUNOLOGY, 102(3), 2001, pp. 323-330

Abstract

Following skin sensitization a proportion of epidermal Langerhans cells (LC) are stimulated to leave the skin and to migrate, via efferent lymphatics, to draining lymph nodes where they accumulate as immunostimulatory dendritic cells (DC). It has been demonstrated previously that tumour necrosis factor-alpha (TNF-alpha), an inducible product of epidermal keratinocytes, and interleukin (IL)-1 beta produced exclusively by LC in murine epidermis. provide important signals for the initiation of this response. Recently. it has been demonstrated that IL-18. a cytokine produced by both LC and keratinocytes within the epidermis, may also participate in immune responses induced following skin sensitization. In the present investigations. the ability of IL-18 to contribute to the regulation of LC migration and the accumulation of DC in draining lymph nodes has been examined. It was round that, like IL-1 beta, IL-18 administered intradermally to mice resulted in a significant reduction in epidermal major histocompatibility complex (MHC) class II+ LC densities and a marked increase in lymph node DC numbers, Using neutralizing anti-TNF-alpha and blocking anti-type I IL-1 receptor (IL-1RI) antibodies. it was shown also that the: induction by IL-18 of both LC mobilization and DC accumulation in regional lymph nodes was dependent upon availability of TNF-alpha and the integrity of IL-1RI signalling. Furthermore, using IL-1 beta converting enzyme (caspase-1) knockout mice, IL-18-induced LC migration was found to have a mandatory requirement For active IL-1 beta. Importantly, not only was IL-18 able to contribute to the regulation of LC migration, it was found to be essential fur the manifestation of these processes in response to topical sensitization with the contact allergen oxazolone.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 04:03:21