Abstract
Ability to make an optimal immune response to vaccines and infectious agents declines with age in humans and animal models. Recent advances have shown intrinsic B cell defects in aged mice and humans, including decreases in Ig class switch recombination (CSR), activation-induced cytidine deaminase (AID), and E47 transcription factor. Effects on somatic hypermutation (SHM) have been varied depending on the system studied. Increase of AID in mice has shown improved CSR but not SHM. The reported microarray analysis of human B cell subsets may now be used to delineate B cell defects with aging and all the advances presented should lead to selecting agents for improved immune response in the elderly.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Aging / immunology*
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Aging / metabolism
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Aging / pathology
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Animals
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B-Lymphocytes / immunology
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B-Lymphocytes / metabolism*
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B-Lymphocytes / pathology
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Cytidine Deaminase / genetics
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Cytidine Deaminase / immunology
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Cytidine Deaminase / metabolism*
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Gene Expression Regulation / immunology
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Humans
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Immune Tolerance*
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Immunoglobulin Class Switching
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Mice
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Somatic Hypermutation, Immunoglobulin
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TCF Transcription Factors / genetics
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TCF Transcription Factors / immunology
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TCF Transcription Factors / metabolism*
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Transcription Factor 7-Like 1 Protein
Substances
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TCF Transcription Factors
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TCF7L1 protein, human
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Tcf7l1 protein, mouse
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Transcription Factor 7-Like 1 Protein
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AICDA (activation-induced cytidine deaminase)
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Cytidine Deaminase