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Titolo:
Intact B cell tolerance in the absence of the first component of the classical complement pathway
Autore:
Cutler, AJ; Cornall, RJ; Ferry, H; Manderson, AP; Botto, M; Walport, MJ;
Indirizzi:
Imperial Coll, Sch Med, Div Med, Rheumatol Sect, London W12 0NN, England Imperial Coll London England W12 0NN matol Sect, London W12 0NN, England Univ Oxford, John Radcliffe Hosp, Nuffield Dept Med, Headington, England Univ Oxford Headington England , Nuffield Dept Med, Headington, England Australian Natl Univ, John Curtin Sch Med Res, Div Cell Biol & Immunol, Canberra, ACT 2601, Australia Australian Natl Univ Canberra ACT Australia 2601 rra, ACT 2601, Australia
Titolo Testata:
EUROPEAN JOURNAL OF IMMUNOLOGY
fascicolo: 7, volume: 31, anno: 2001,
pagine: 2087 - 2093
SICI:
0014-2980(200107)31:7<2087:IBCTIT>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
T-DEPENDENT ANTIGEN; IMMUNE-RESPONSE; LYMPHOCYTES-B; SELF-TOLERANCE; DENDRITIC CELL; RECEPTORS; INDUCTION; MICE; ERYTHEMATOSUS; KERATINOCYTES;
Keywords:
complement; B lymphocyte; tolerance; lupus; transgenic;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Walport, MJ Imperial Coll, Sch Med, Div Med, Rheumatol Sect, Hammersmith Campus,Du Cane Rd, London W12 0NN, England Imperial Coll Hammersmith Campus,Du Cane Rd London England W12 0NN
Citazione:
A.J. Cutler et al., "Intact B cell tolerance in the absence of the first component of the classical complement pathway", EUR J IMMUN, 31(7), 2001, pp. 2087-2093

Abstract

A critical role for complement in the regulation of self tolerance has been proposed to explain the strong association between complement deficiency and autoimmunity. To elucidate the role of the classical pathway of complement in the maintenance of B cell tolerance, Clq deficient (C1qa-/-) mice were bred with anti-hen egg lysozyme (MEL) immunoglobulin (Ig(HEL)) and soluble MEL (sHEL) transgenic mice. B cell tolerance was intact in C1qa-/- mice. In vivo, double-transgenic (Ig(HEL)/sHEL) C1qa-/- and wild-type control mice down-regulated surface immunoglobulin expression on splenocytes and equivalent numbers of MEL-binding B cells accumulated in the periphery. Maturation of B cells, evidenced by CD21 expression, was retarded to the same extent and at a similar time point. The frequency of anti-MEL-producing plasma cells and serum levels of anti-MEL immunoglobulin were comparably reduced in control and C1qa-/- double-transgenic mice compared to control Ig(HEL) and C1qa-/- Ig(HEL) mice. Furthermore, splenocytes from double-transgenic C1qa-/- or wild-type mice did not modulate intracellular calcium levels after stimulation with MEL in vitro. These data demonstrate that a stable form ofB cell anergy persists in the periphery of C1qa-/- mice, suggesting that activation of the classical pathway by C1q is not essential for the maintenance of B cell tolerance in this transgenic model.

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Documento generato il 26/11/20 alle ore 11:42:57