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Titolo:
ORAL TOLERANCE TO LOW-DOSE BETA(2)-GLYCOPROTEIN - I - IMMUNOMODULATION OF EXPERIMENTAL ANTIPHOSPHOLIPID SYNDROME
Autore:
BLANK M; GEORGE J; BARAK V; TINCANI A; KOIKE T; SHOENFELD Y;
Indirizzi:
CHAIM SHEBA MED CTR,DEPT MED B,AUTOIMMUNE DIS RES UNIT IL-52621 TEL HASHOMER ISRAEL CHAIM SHEBA MED CTR,DEPT MED B,AUTOIMMUNE DIS RES UNIT IL-52621 TEL HASHOMER ISRAEL HADASSAH MED CTR,DEPT ONCOL,IMMUNOL LAB DIAG IL-91120 JERUSALEM ISRAEL TEL AVIV UNIV,SACKLER FAC MED IL-69978 TEL AVIV ISRAEL HOKKAIDO UNIV,SCH MED,DEPT MED 2 SAPPORO HOKKAIDO 060 JAPAN SPEDALI CIVIL BRESCIA,CLIN IMMUNOL UNIT I-25125 BRESCIA ITALY
Titolo Testata:
The Journal of immunology (1950)
fascicolo: 10, volume: 161, anno: 1998,
pagine: 5303 - 5312
SICI:
0022-1767(1998)161:10<5303:OTTLB->2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
MYELIN BASIC-PROTEIN; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; SUPPRESSOR T-CELLS; GROWTH-FACTOR-BETA; SYSTEMIC LUPUS-ERYTHEMATOSUS; MICE FOLLOWING IMMUNIZATION; GLYCOPROTEIN-I; IMMUNOLOGICAL-TOLERANCE; APOLIPOPROTEIN-H; IMMUNE-RESPONSES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
50
Recensione:
Indirizzi per estratti:
Citazione:
M. Blank et al., "ORAL TOLERANCE TO LOW-DOSE BETA(2)-GLYCOPROTEIN - I - IMMUNOMODULATION OF EXPERIMENTAL ANTIPHOSPHOLIPID SYNDROME", The Journal of immunology (1950), 161(10), 1998, pp. 5303-5312

Abstract

Oral tolerance was induced in BALB/c mice by feeding low dose beta(2)-glycoprotein I (beta(2)GPI). The beta(2)GPI-fed mice did not develop serologic and clinical markers of experimental antiphospholipid syndrome (APS) upon immunization with the autoantigen, The treated group wascharacterized by low titers of serum anti-beta(2)GPI and anticardiolipin Abs in the serum, lack of fetal resorptions, low incidence of thrombocytopenia, and normal aPTT (activated partial thromboplastin time) values. beta(2)GPI given orally before priming with beta(2)GPI resulted in complete prevention of experimental APS development; beta(2)GPI given at an early stage of the disease reduced clinical manifestations. However, administration of beta(2)GPI 70 days postimmunization bad a less significant effect on disease expression. Tolerized mice exhibited a diminished T lymphocyte proliferation response to beta(2)GPI in comparison with beta(2)GPI-immunized mice fed with OVA, When nontolerantbeta(2)GPI-primed T lymphocytes were mixed with T lymphocytes derivedfrom tolerized mice, a significant inhibition of proliferation upon exposure to beta(2)GPI was observed. The induction of suppression was beta(2)GPI specific and driven, as well as TGF-beta mediated, The beta(2)GPI-specific response of T lymphocytes from the beta(2)GPI-fed mice was reversed by anti-TGF-beta Abs, The tolerance was adoptively transferred by CD8(+) T cells from the tolerized mice into naive mice. ThoseCD8(+) cells were MHC class I restricted, found to secrete TGF-beta, and had no cytolytic activity. Oral administration of beta(2)GPI suppressed priming of CTLs in the recipient mice. In sum, beta(2)GPI-induced oral tolerance has an immunomodulatory effect in experimental APS, demonstrating the importance of beta(2)GPI in the pathogenesis of the disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 11:54:43