Suscripción a Biblioteca: Guest
Portal Digitalde Biblioteca Digital eLibros Revistas Referencias y Libros de Ponencias Colecciones
Critical Reviews™ in Immunology
Factor de Impacto: 1.352 Factor de Impacto de 5 años: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN Imprimir: 1040-8401
ISSN En Línea: 2162-6472

Volumes:
Volumen 39, 2019 Volumen 38, 2018 Volumen 37, 2017 Volumen 36, 2016 Volumen 35, 2015 Volumen 34, 2014 Volumen 33, 2013 Volumen 32, 2012 Volumen 31, 2011 Volumen 30, 2010 Volumen 29, 2009 Volumen 28, 2008 Volumen 27, 2007 Volumen 26, 2006 Volumen 25, 2005 Volumen 24, 2004 Volumen 23, 2003 Volumen 22, 2002 Volumen 21, 2001 Volumen 20, 2000 Volumen 19, 1999 Volumen 18, 1998 Volumen 17, 1997 Volumen 16, 1996 Volumen 15, 1995 Volumen 14, 1994

Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v31.i1.30
pages 31-42

CD5 Expression in B Cells from Patients with Systemic Lupus Erythematosus

Pierre Youinou
Laboratory of Immunology, European University of Brittany, and Brest University Medical School Hospital
Yves Renaudineau
Laboratory of Immunology, European University of Brittany, and Brest University Medical School Hospital

SINOPSIS

The recently recognized importance of B cells in systemic lupus erythematosus (SLE) raises the question as to whether those expressing CD5 predominate over the remaining B lymphocytes in the pathophysiology of this disease. Owing to their B B-cell receptor (BCR) polyspecificity, autoantibody production has been originally ascribed to CD5-positive B1 lymphocytes. Instead, it has since been established that high-affinity autoantibodies derive from CD5-negative B2 cells. Even worse, in the light of current findings, CD5-positive B cells have been considered to play a paradoxical role in preventing, rather than inducing, autoimmunity. In this context, there is evidence that the membrane expression of CD5 is regulated, and, to this end, a genetic mechanism has been described, based on the selection between exon 1A (E1A) and exon 1B (E1B). The full-length protein variant, encoded by E1A-cd5, translocates the phosphatase SHP-1 to the vicinity of the BCR, raises its threshold, and thereby limits the response of autoreactive B cells. In contrast, the truncated variant, encoded by E1B-cd5, remains in the cytoplasm, along with SHP1. Normally, EIB E1B is silenced by methylation and its product degraded in the proteosomes. Hence, a defect in the DNA methyl transfer favors the development of SLE, by preventing the effects of SHP-1.


Articles with similar content:

A Common Regulator of Cold and Radiation Response in Escherichia coli
Journal of Environmental Pathology, Toxicology and Oncology, Vol.20, 2001, issue 1
Vibhav R. Sanzgiri, Suhas Mangoli, Suresh K. Mahajan
T- and B-Cell Abnormalities in Systemic Lupus Erythematosus
Critical Reviews™ in Immunology, Vol.25, 2005, issue 2
Gyorgy Nagy, Agnes Koncz, Andras Perl
The Role of Pax3 and Pax7 in Development and Cancer
Critical Reviews™ in Oncogenesis, Vol.9, 1998, issue 2
Ahmed Mansouri
Expression and Function of Recombination Activating Genes in Mature В Cells
Critical Reviews™ in Immunology, Vol.18, 1998, issue 3
Masaki Hikida, Hitoshi Ohmori
The Regulation of Endotoxin Tolerance and its Impact on Macrophage Activation
Critical Reviews™ in Immunology, Vol.35, 2015, issue 4
Patricia E. Collins , Ruaidhri J. Carmody