- Authors:
-
Tavares, Rm; Turer, Ee; Liu, Cl; Advincula, R; Scapini, Patrizia; Rhee, L; Barrera, J; Lowell, Ca; Utz, Pj; Malynn, Ba; Ma, A.
- Title:
-
The Ubiquitin Modifying Enzyme A20 Restricts B Cell Survival and Prevents Autoimmunity
- Year:
-
2010
- Type of item:
-
Articolo in Rivista
- Tipologia ANVUR:
- Articolo su rivista
- Language:
-
Inglese
- Format:
-
A Stampa
- Referee:
-
Sì
- Name of journal:
- Immunity
- ISSN of journal:
- 1074-7613
- N° Volume:
-
33
- Number or Folder:
-
2
- Page numbers:
-
181-191
- Keyword:
-
MOLIMMUNO; CELLIMMUNO; SIGNALING
- Short description of contents:
- 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.
- Product ID:
-
57607
- Handle IRIS:
-
11562/345450
- Deposited On:
-
October 13, 2010
- Last Modified:
-
November 15, 2022
- Bibliographic citation:
-
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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