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Mechanisms for Decreased Function of B Cells in Aged Mice and Humans¹

Daniela Frasca^*,, Ana Marie Landin^*, Richard L. Riley^* and Bonnie B. Blomberg^2,*

^* Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33101; and Graduate School of Cell Biology and Development, University of Rome La Sapienza, Rome, Italy

The immune system has been known for some time to be compromised in aged individuals, e.g., both mice and humans, and in both humoral and cellular responses. Our studies have begun to elucidate intrinsic B lymphocyte defects in Ig class switch recombination, activation-induced cytidine deaminase, and E47 transcription factor expression. These defects occur in both mice and humans. Our studies have also shown that tristetraprolin is one of the key players in regulating the decreased E47 mRNA stability in aged B lymphocytes. These and current studies should lead to improvements in B lymphocyte function in aged populations.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants AG-17618, AG-23717, and AG-28586 (to B.B.B.) and AG-025256 and AI-064591 (to R.L.R.).

² Address correspondence and reprint requests to Dr. Bonnie Blomberg, Department of Microbiology and Immunology, University of Miami Miller School of Medicine, P.O. Box 016960 (R-138), Miami, FL 33101. E-mail address: bblomber{at}med.miami.edu

³ Abbreviations used in this paper: SHM, somatic hypermutation; AID, activation-induced cytidine deaminase; ARE, adenylate/uridylate-rich elements; BAFF, B cell-activating factor; CSR, class switch recombination; GC, germinal center; S region, switch region; TTP, tristetraprolin; UTR, untranslated region.