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Titolo:
Regulation of epidermal Langerhans cell migration by lactoferrin
Autore:
Cumberbatch, M; Dearman, RJ; Uribe-Luna, S; Headon, DR; Ward, PP; Conneely, OM; Kimber, I;
Indirizzi:
Zeneca Cent Toxicol Lab, Macclesfield SK10 4TJ, Cheshire, England Zeneca Cent Toxicol Lab Macclesfield Cheshire England SK10 4TJ e, England Baylor Coll Med, Dept Cell Biol, Houston, TX 77030 USA Baylor Coll Med Houston TX USA 77030 ept Cell Biol, Houston, TX 77030 USA Agennix Inc, Houston, TX USA Agennix Inc Houston TX USAAgennix Inc, Houston, TX USA
Titolo Testata:
IMMUNOLOGY
fascicolo: 1, volume: 100, anno: 2000,
pagine: 21 - 28
SICI:
0019-2805(200005)100:1<21:ROELCM>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
NECROSIS-FACTOR-ALPHA; DRAINING LYMPH-NODES; THYMIDINE INCORPORATION; GRANULOCYTE-MACROPHAGE; HUMAN LACTOTRANSFERRIN; CONTACT SENSITIZATION; DENDRITIC CELLS; INDUCTION-PHASE; GENE-EXPRESSION; BINDING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Cumberbatch, M Zeneca Cent Toxicol Lab, Macclesfield SK10 4TJ, Cheshire, England Zeneca Cent Toxicol Lab Macclesfield Cheshire England SK10 4TJ
Citazione:
M. Cumberbatch et al., "Regulation of epidermal Langerhans cell migration by lactoferrin", IMMUNOLOGY, 100(1), 2000, pp. 21-28

Abstract

Lactoferrin (LF) is a member of the transferrin family of iron-binding glycoproteins to which several anti-inflammatory functions have been ascribed. LF has been shown to down-regulate expression of the pro-inflammatory cytokine tumour necrosis factor-alpha (TNF-alpha), although the possibility hasbeen raised that the activity of LF in this regard was indirect and secondary to its ability to bind to and inactivate the bacterial lipopolysaccharide (LPS) used to induce cytokine production. However, the identification ofputative membrane receptors for LF raises the possibility that the interaction of LF with its receptor may be one important route through which this protein exerts anti-inflammatory activity. In the present investigations the biological properties of LF have been examined in a model of cutaneous immune function where the allergen-induced migration of epidermal Langerhans cells (LC) from the skin and their subsequent accumulation as dendritic cells (DC) in skin-draining lymph nodes are known to be dependent upon the de novo synthesis of TNF-alpha, but independent of exogenous LPS. Consistent with the protein having direct anti-inflammatory properties, it was found that the intradermal injection of recombinant murine LF (either iron-saturated or iron-depleted LF) inhibited significantly allergen (oxazolone) -induced LC migration and DC accumulation. That these inhibitory effects were secondary to the inhibition of local TNF-alpha synthesis was suggested by the findings that first, LF was unable to inhibit LC migration induced by intradermal injection of TNF-alpha itself, and second, that migration stimulated by local administration of another epidermal cytokine, interleukin 1 beta, which is also dependent upon TNF-alpha production, was impaired significantly by prior treatment with LF. Finally, immunohistochemical analyses demonstrated the presence of LF in skin, associated primarily with keratinocytes. Collectively these data support the possession by LF of direct immunomodulatory and/or anti-inflammatory activity, probably associated in this case with inhibition of cytokine production. Furthermore, the results suggest that as a constituent of normal skin, LF may play a role in homeostatic regulation of cutaneous immune function.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 12:15:55