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Titolo:
CD19 can regulate B lymphocyte signal transduction independent of complement activation
Autore:
Hasegawa, M; Fujimoto, M; Poe, JC; Steeber, DA; Tedder, TF;
Indirizzi:
Duke Univ, Med Ctr, Dept Immunol, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 Med Ctr, Dept Immunol, Durham, NC 27710 USA
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 6, volume: 167, anno: 2001,
pagine: 3190 - 3200
SICI:
0022-1767(20010915)167:6<3190:CCRBLS>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
LYN-DEFICIENT MICE; SYSTEMIC LUPUS-ERYTHEMATOSUS; FOLLICULAR DENDRITIC CELLS; TYROSINE KINASE ACTIVATION; HUMORAL IMMUNE-RESPONSES; T-DEPENDENT ANTIGEN; EPSTEIN-BARR-VIRUS; ANTIBODY-RESPONSE; CYTOPLASMIC DOMAIN; RECEPTOR TYPE-2;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
72
Recensione:
Indirizzi per estratti:
Indirizzo: Tedder, TF Duke Univ, Med Ctr, Dept Immunol, Box 3010, Durham, NC 27710 USA Duke Univ Box 3010 Durham NC USA 27710 10, Durham, NC 27710 USA
Citazione:
M. Hasegawa et al., "CD19 can regulate B lymphocyte signal transduction independent of complement activation", J IMMUNOL, 167(6), 2001, pp. 3190-3200

Abstract

B lymphocytes are critically regulated by signals transduced through the CD19-CD21 cell surface receptor complex, where complement C3d binding to CD21 supplies an already characterized ligand. To determine the extent that CD19 function is controlled by complement activation, CD19-deficient mice (that are hyporesponsive to transmembrane signals) and mice overexpressing CD19 (that are hyperresponsive) were crossed with CD21- and C3-deficient mice. Cell surface CD19 and CD21 expression were significantly affected by the loss of CD21 and C3 expression, respectively. Mature B cells from CD21-deficient littermates had similar to 36% higher cell surface CD19 expression, whereas CD21/35 expression was increased by similar to 45% on B cells from C3-deficient mice. Negative regulation of CD19 and CD21 expression by CD21 and C3, respectively, may be functionally significant because small increasesin cell surface CD19 overexpression can predispose to autoimmunity. Otherwise, B cell development and function in CD19-deficient and -overexpressing mice were not significantly affected by a simultaneous loss of CD21 expression. Although CD21-deficient mice were found to express a hypomorphic cell surface CD21 protein at low levels that associated with mouse CD19, C3 deficiency did not significantly affect B cell development and function in CD19-deficient or -overexpressing mice. These results, and the severe phenotypeexhibited by CD19-deficient mice compared with CD21- or C3-deficient mice,collectively demonstrate that CD19 can regulate B cell signaling thresholds independent of CD21 engagement and complement activation.

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Documento generato il 01/12/20 alle ore 22:59:24