Pubblicazioni

Autori:

Tavares, Rm; Turer, Ee; Liu, Cl; Advincula, R; Scapini, Patrizia; Rhee, L; Barrera, J; Lowell, Ca; Utz, Pj; Malynn, Ba; Ma, A.

Titolo:

The Ubiquitin Modifying Enzyme A20 Restricts B Cell Survival and Prevents Autoimmunity

Anno:

2010

Tipologia prodotto:

Articolo in Rivista

Tipologia ANVUR:

Articolo su rivista

Lingua:

Inglese

Formato:

A Stampa

Referee:

Sì

Nome rivista:

Immunity

ISSN Rivista:

1074-7613

N° Volume:

33

Numero o Fascicolo:

2

Intervallo pagine:

181-191

Parole chiave:

MOLIMMUNO; CELLIMMUNO; SIGNALING

Breve descrizione dei contenuti:

A20 is a ubiquitin modifying enzyme that restricts NF-kappaB signals and protects cells against tumor necrosis factor (TNF)-induced programmed cell death. Given recent data linking A20 (TNFAIP3) with human B cell lymphomas and systemic lupus erythematosus (SLE), we have generated mice bearing a floxed allele of Tnfaip3 to interrogate A20's roles in regulating B cell functions. A20-deficient B cells are hyperresponsive to multiple stimuli and display exaggerated NF-kappaB responses to CD40-induced signals. Mice expressing absent or hypomorphic amounts of A20 in B cells possess elevated numbers of germinal center B cells, autoantibodies, and glomerular immunoglobulin deposits. A20-deficient B cells are resistant to Fas-mediated cell death, probably due to increased expression of NF-kappaB-dependent antiapoptotic proteins such as Bcl-x. These findings show that A20 can restrict B cell survival, whereas A20 protects other cells from TNF-induced cell death. Our studies demonstrate how reduced A20 expression predisposes to autoimmunity.

Id prodotto:

57607

Handle IRIS:

11562/345450

depositato il:

13 ottobre 2010

ultima modifica:

15 novembre 2022

Citazione bibliografica:

Tavares, Rm; Turer, Ee; Liu, Cl; Advincula, R; Scapini, Patrizia; Rhee, L; Barrera, J; Lowell, Ca; Utz, Pj; Malynn, Ba; Ma, A., The Ubiquitin Modifying Enzyme A20 Restricts B Cell Survival and Prevents Autoimmunity «Immunity» , vol. 33 , n. 2 , 2010 , pp. 181-191

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