Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
NEGATIVE SELECTION OF HUMAN GERMINAL CENTER B-CELLS BY PROLONGED BCR CROSS-LINKING
Autore:
GALIBERT L; BURDIN N; BARTHELEMY C; MEFFRE G; DURAND I; GARCIA E; GARRONE P; ROUSSET F; BANCHEREAU J; LIU YJ;
Indirizzi:
SCHERING PLOUGH SPA,LAB IMMUNOL RES,27 CHEMIN PEUPLIERS,BP 11 F-69571DARDILLY FRANCE SCHERING PLOUGH SPA,LAB IMMUNOL RES F-69571 DARDILLY FRANCE
Titolo Testata:
The Journal of experimental medicine
fascicolo: 5, volume: 183, anno: 1996,
pagine: 2075 - 2085
SICI:
0022-1007(1996)183:5<2075:NSOHGC>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
FREE CALCIUM; LYMPHOCYTES-B; T-CELLS; ANTIGEN; ACTIVATION; HETEROGENEITY; STIMULATION; TOLERANCE; MECHANISM; SUBSETS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
50
Recensione:
Indirizzi per estratti:
Citazione:
L. Galibert et al., "NEGATIVE SELECTION OF HUMAN GERMINAL CENTER B-CELLS BY PROLONGED BCR CROSS-LINKING", The Journal of experimental medicine, 183(5), 1996, pp. 2075-2085

Abstract

The antigen receptors on T and B lymphocytes can transduce both agonist and antagonist signals leading either to activation/survival or anergy/death. The outcome of B lymphocyte antigen receptor (BCR) triggering depends upon multiple parameters which include (a) antigen concentration and valency, (b) duration of BCR occupancy, (c) receptor affinity, and (d) B cell differentiation stages. Herein, using anti-immunoglobulin kappa and lambda light chain antibodies, we analyzed the response of human naive, germinal center (GC) or memory B cells to BCR crosslinking regardless of heavy chain Ig isotype or intrinsic BCR specificity. We show that after CD40-activation, anti-BCR(kappa+lambda) can elicit an intracellular calcium flux on both GC and non-GC cells. However, prolonged BCR cross-linking induces death of CD40-activated GC B cells but enhances proliferation of naive or memory cells. Anti-kappa antibody only kills kappa(+) GC B cells without affecting surrounding lambda(+) GC B cells, thus demonstrating that BCR-mediated killing of GC B lymphocytes is a direct effect that does not involve a paracrine mechanism. BCR-mediated killing of CD40-activatcd GC B cells could be partially antagonized by the addition of IL-4. Moreover, in the presence of IL-4, prestimulation through CD40 could prevent subsequent anti-Ig-mediated cell death, suggesting a specific role of this combination inselection of GC B cells. This report provides evidence that in human,susceptibility to BCR killing is regulated along peripheral B cell differentiation pathway.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 18:24:00