Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
TGF-beta-producing CD4(+) mediastinal lymph node cells obtained from mice tracheally tolerized to ovalbumin (OVA) suppress both Th1-and Th2-induced cutaneous inflammatory responses to OVA by different mechanisms
Autore:
Terui, T; Sano, K; Shirota, H; Kunikata, N; Ozawa, M; Okada, M; Honda, M; Tamura, G; Tagami, H;
Indirizzi:
Tohoku Univ, Sch Med, Dept Dermatol, Aoba Ku, Sendai, Miyagi 9808574, Japan Tohoku Univ Sendai Miyagi Japan 9808574 Ku, Sendai, Miyagi 9808574, Japan Tohoku Univ, Sch Med, Dept Internal Med 1, Aoba Ku, Sendai, Miyagi 9808574, Japan Tohoku Univ Sendai Miyagi Japan 9808574 Ku, Sendai, Miyagi 9808574, Japan
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 7, volume: 167, anno: 2001,
pagine: 3661 - 3667
SICI:
0022-1767(20011001)167:7<3661:TCMLNC>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; COLLAGEN-INDUCED ARTHRITIS; DELTA T-CELLS; ORAL TOLERANCE; ATOPIC-DERMATITIS; IMMUNE DEVIATION; INTERFERON-GAMMA; INHALED ANTIGEN; TRANSGENIC MICE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Terui, T Tohoku Univ, Sch Med, Dept Dermatol, Aoba Ku, Seiryo Machi 1-1, Sendai, Miyagi 9808574, Japan Tohoku Univ Seiryo Machi 1-1 Sendai Miyagi Japan 9808574 4, Japan
Citazione:
T. Terui et al., "TGF-beta-producing CD4(+) mediastinal lymph node cells obtained from mice tracheally tolerized to ovalbumin (OVA) suppress both Th1-and Th2-induced cutaneous inflammatory responses to OVA by different mechanisms", J IMMUNOL, 167(7), 2001, pp. 3661-3667

Abstract

Advances in the treatment of allergic disorders require elucidation of theautoregulatory immune systems induced in averting detrimental inflammatoryresponses against invading foreign Ags. We previously reported that excessive Ags intruding through the airway mucosa induce a subset of regulatory CD4(+) T cells secreting TGF-beta in the regional mediastinal lymph nodes (MLNs), which inhibits Th2 cells and subsequent eosinophilic inflammation in the trachea. In the present experiments we examined whether and in what mechanisms TGF-beta -secreting CD4(+) T cells in the MLNs regulate Th cell-mediated skin inflammation using a previously established murine model. Th1 orTh2 cells injected s.c. into ear lobes of naive mice induced swelling, whereas the concomitant local injection of MLN cells suppressed the inflammation. The suppressor activities of MLN cells were markedly neutralized by anti-TGF-beta mAb and were mimicked by rTGF-beta. The MLN cell- and rTGF-beta -induced inhibition was reversed by anti-IL-10 mAb significantly in Th1-induced inflammation and only partially in Th2-induced inflammation. rIL-10 reduced Th-induced ear swelling, although higher doses of rIL-10 were required in Th2-induced one. Thus, allergen-specific TGF-beta -producing CD4(+) T cells induced in the respiratory tract controlled cutaneous inflammatory responses by Th1 or Th2 cells either directly by TGF-beta or indirectly through IL-10 induction. From a clinical standpoint, these observations might explain the mechanism of spontaneous regression in some patients with atopic dermatitis, which exhibits both Th1- and Th2-mediated skin inflammation in response to airborne protein Ags.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 23:31:49