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Titolo:
Complement opsonization is required for presentation of immune complexes by resting peripheral blood B cells
Autore:
Boackle, SA; Morris, MA; Holers, VM; Karp, DR;
Indirizzi:
Univ Texas, SW Med Ctr, Simmons Arthrit Res Ctr, Dallas, TX 75235 USA UnivTexas Dallas TX USA 75235 mons Arthrit Res Ctr, Dallas, TX 75235 USA Univ Colorado, Hlth Sci Ctr, Dept Med, Denver, CO 80262 USA Univ ColoradoDenver CO USA 80262 Sci Ctr, Dept Med, Denver, CO 80262 USA UnivUSAlorado, Hlth Sci Ctr, Dept Immunol, Div Rheumatol, Denver, CO 80262Univ Colorado Denver CO USA 80262 mmunol, Div Rheumatol, Denver, CO 80262
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 12, volume: 161, anno: 1998,
pagine: 6537 - 6543
SICI:
0022-1767(199812)161:12<6537:COIRFP>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
SYSTEMIC LUPUS-ERYTHEMATOSUS; T-DEPENDENT ANTIGEN; HUMAN LYMPHOCYTES-B; FC-GAMMA-RII; MONOCLONAL-ANTIBODIES; NATURAL ANTIBODY; RECEPTOR TYPE-2; IN-VIVO; EXPRESSION; ACTIVATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Karp, DR Univlas,as, SW Med Ctr, Simmons Arthrit Res Ctr, 5323 Harry HinesBlvd, Dal Univ Texas 5323 Harry Hines Blvd Dallas TX USA 75235 es Blvd, Dal
Citazione:
S.A. Boackle et al., "Complement opsonization is required for presentation of immune complexes by resting peripheral blood B cells", J IMMUNOL, 161(12), 1998, pp. 6537-6543

Abstract

Complement receptor 2 (CD21, CR2) is a B cell receptor for complement degradation products bound to Ag or immune complexes. The role of CD21 in mediating Ag presentation of soluble immune complexes by resting B cells was studied. Complement-coated immune complexes were formed by the incubation of influenza virus with serum from immune donors. These complexes bound to peripheral blood B cells in a complement-dependent manner. The binding requiredCD21 or, to a lesser extent, complement receptor 1 (CR1, CD35), B cells pulsed with immune complexes containing complement elicited a response from apanel of influenza-specific T cell clones, while those pulsed with immune complexes formed in the absence of complement did not. The expression of the early activation marker CD69 and the costimulatory molecule CD86 were notinduced by CD21 ligation alone, suggesting that CD21-mediated Ag presentation occurs independently of B cell activation. Up-regulation of these markers required exposure to T cell factors elicited by the recognition of Ag derived from complement-containing immune complexes. These findings suggest that binding of Ag to CD21 enables Ag-nonspecific B cells to participate in the activation of Ag-specific T cells in a process that occurs independently of well-characterized B cell activation events.

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Documento generato il 05/12/20 alle ore 00:11:26