Abonnement à la biblothèque: Guest
Portail numérique Bibliothèque numérique eBooks Revues Références et comptes rendus Collections
Critical Reviews™ in Immunology
Facteur d'impact: 1.352 Facteur d'impact sur 5 ans: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN Imprimer: 1040-8401
ISSN En ligne: 2162-6472

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

Interleukin 4–Induced Gene 1 as an Emerging Regulator of B-Cell Biology and its Role in Cutaneous Melanoma
Critical Reviews™ in Immunology, Vol.39, 2019, issue 1
Yolande Richard, Armelle Prevost-Blondel
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
Antigen-Specific B-Lymphocyte Activation
Critical Reviews™ in Immunology, Vol.23, 2003, issue 3
Gail A. Bishop, Sokol A. Haxhinasto, Bruce S. Hostager, Laura L. Stunz
Role of Inflammation Amplifier-Induced Growth Factor Expression in the Development of Inflammatory Diseases
Critical Reviews™ in Immunology, Vol.35, 2015, issue 5
Yasunobu Arima, Daisuke Kamimura, Masaaki Murakami, Toru Atsumi, Ikuma Nakagawa
Plasma Cell Formation, Secretion, and Persistence: The Short and the Long of It
Critical Reviews™ in Immunology, Vol.34, 2014, issue 6
Christine Milcarek, Ian Bayles