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

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.v24.i5.10
24 pages

Effect of Age on the Immunoglobulin Class Switch

Daniela Frasca
Department of Microbiology and Immunology, University of Miami School of Medicine, P.O. Box 016960 (R-138), Miami, FL33101
Richard L. Riley
Department of Microbiology and Immunology, University of Miami School of Medicine, P.O. Box 016960 (R-138), Miami, FL33101
Bonnie B. Blomberg
Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33101, USA


Aging represents a complex remodelling in which both specific and innate immunity deteriorate. Age-related changes in humoral immunity involve reduced vaccine responses and increased production of auto-antibodies. Although T-cell alterations play a significant role in age-related humoral immune changes, alterations in B cells also occur. In this review, we provide an overview of age-related changes in B-cell functions and markers, including transcription factors, and also discuss controversies in the field of B-cell aging. We summarize our recent results, showing that splenic B cells from senescent mice are deficient in production of secondary isotypes (IgG1, IgG2a, IgG3, IgE), class switch recombination (CSR), and expression of the transcription factor E47. We also demonstrate that there is more Id2 (a negative regulator of E47) in old activated B cells. E47 is required for CSR, at least in part, via expression of activation-induced cytidine deaminase (AID). Our studies show that impaired induction of E47, and, subsequently, AID, contribute to poor CSR and production of secondary isotypes in senescence. We also present new data indicating the absence of DNA switch region excision circles for CSR in old activated B cells, confirming the location of the defect at the DNA endonucleolytic step. And, finally, we show that there is no change in NF-κB or Blimp-1 in old vs young stimulated B cells.

Articles with similar content:

Mechanism of Activation-Induced Cell Death of T Cells and Regulation of FasL Expression
Critical Reviews™ in Immunology, Vol.34, 2014, issue 4
Akiko Yamada, Yasusei Kudo, Yoshio Hayashi, Naozumi Ishimaru, Rieko Arakaki
Regulation of aicda Expression and AID Activity: Relevance to Somatic Hypermutation and Class Switch DNA Recombination
Critical Reviews™ in Immunology, Vol.27, 2007, issue 4
Ahmed Al-Qahtani, Seok-Rae Park, Egest J. Pone, Paolo Casali, Hong Zan, Zhenming Xu
The Role of CARMA1 in T Cells
Critical Reviews™ in Immunology, Vol.33, 2013, issue 3
Marly I. Roche, Benjamin D. Medoff, Ravisankar A. Ramadas
Implication of Cyclin D1 in Malignant Lymphoma
Critical Reviews™ in Oncogenesis, Vol.7, 1996, issue 3-4
Ruth Rimokh, Dominique Leroux, Mary Callanan, Jean-Pierre Magaud
Homeostatic Regulation of Aging and Rejuvenation in the B Lineage Cells
Critical Reviews™ in Immunology, Vol.33, 2013, issue 1
Doron Melamed