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Titolo:
xid mice reveal the interplay of homeostasis and Bruton's tyrosine kinase-mediated selection at multiple stages of B cell development
Autore:
Cancro, MP; Sah, AP; Levy, SL; Allman, DM; Schmidt, MR; Woodland, RT;
Indirizzi:
Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA UnivPenn Philadelphia PA USA 19104 & Lab Med, Philadelphia, PA 19104 USA Univ Massachusetts, Med Ctr, Dept Mol Genet & Microbiol, Worcester, MA 01655 USA Univ Massachusetts Worcester MA USA 01655 robiol, Worcester, MA 01655 USA
Titolo Testata:
INTERNATIONAL IMMUNOLOGY
fascicolo: 12, volume: 13, anno: 2001,
pagine: 1501 - 1514
SICI:
0953-8178(200112)13:12<1501:XMRTIO>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
X-LINKED AGAMMAGLOBULINEMIA; MOUSE BONE-MARROW; HEAT-STABLE ANTIGEN(HI); NEGATIVE SELECTION; REGULATED EXPRESSION; SIGNAL-TRANSDUCTION; TRANSGENIC MICE; BCL-2 TRANSGENE; LYMPHOCYTES-B; FETAL LIVER;
Keywords:
apoptosis; differentiation; homeostasis; immune deficiency; lymphocyte;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
80
Recensione:
Indirizzi per estratti:
Indirizzo: Cancro, MP Univ Penn, Sch Med, Dept Pathol & Lab Med, 36th & Hamilton Walk, Philadelphia, PA 19104 USA Univ Penn 36th & Hamilton Walk Philadelphia PAUSA 19104 04 USA
Citazione:
M.P. Cancro et al., "xid mice reveal the interplay of homeostasis and Bruton's tyrosine kinase-mediated selection at multiple stages of B cell development", INT IMMUNOL, 13(12), 2001, pp. 1501-1514

Abstract

Human X-linked agammaglobulinemia (XLA) and murine X-linked immune defect (XID) are both immunodeficiencies mediated by mutations in Bruton's tyrosine kinase (Btk), yet the developmental stage(s) affected remain controversial. To further refine the placement of the XID defect(s), we used bromodeoxyuridine labeling to determine turnover, production and transition rates of developing B cell subsets in normal, xid and xid mice expressing a human Bcl-2 transgene (xid/bcl-2). We find the xid mutation manifest at two stages of B cell development. The first is early, reducing pre-B cell production by restricting pro-B to pre-B cell transit. Surprisingly, this impairment isoffset by increased survival of cells progressing from the pre- to immature B cell pool, suggesting that Btk-independent homeostatic mechanisms act to maintain this compartment. The second point of action is late, substantially reducing mature B cell production. Together, these findings reconcile apparent discrepancies in the developmental stage affected by the murine versus human lesions and suggest previously unappreciated homeostatic processes that act at the pre-B to immature B cell transition. Finally, Btk likely functions differently at these two checkpoints, since ectopic Bcl-2 expression fails to directly complement the early xid lesion, yet reverses the defect impeding final B cell maturation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 06:59:23