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Ageing, autoimmunity and arthritis: Senescence of the B cell compartment – implications for humoral immunity

Immunosenescence is associated with a decline in both T and B lymphocyte function. Although aged individuals have normal numbers of B cells in the periphery and are capable of mounting robust humoral responses, the antibodies produced are generally of lower affinity and are less protective than thos...

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Detalles Bibliográficos
Autores principales: Johnson, Sara A, Cambier, John C
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2004
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC464870/
https://www.ncbi.nlm.nih.gov/pubmed/15225355
http://dx.doi.org/10.1186/ar1180
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author Johnson, Sara A
Cambier, John C
author_facet Johnson, Sara A
Cambier, John C
author_sort Johnson, Sara A
collection PubMed
description Immunosenescence is associated with a decline in both T and B lymphocyte function. Although aged individuals have normal numbers of B cells in the periphery and are capable of mounting robust humoral responses, the antibodies produced are generally of lower affinity and are less protective than those produced by young animals. Here we review multiple studies that address the mechanisms that contribute to this decline. Taken together, these studies suggest that age-associated loss of the ability to generate protective humoral immunity results in part from reduced B lymphopoiesis. As the output of new, naïve B cells declines, homeostatic pressures presumably force the filling of the peripheral B cell pool by long-lived antigen-experienced cells. Because the antibody repertoire of these cells is restricted by previous antigenic experience, they make poor quality responses to new immunologic insults.
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spelling pubmed-4648702004-07-16 Ageing, autoimmunity and arthritis: Senescence of the B cell compartment – implications for humoral immunity Johnson, Sara A Cambier, John C Arthritis Res Ther Review Immunosenescence is associated with a decline in both T and B lymphocyte function. Although aged individuals have normal numbers of B cells in the periphery and are capable of mounting robust humoral responses, the antibodies produced are generally of lower affinity and are less protective than those produced by young animals. Here we review multiple studies that address the mechanisms that contribute to this decline. Taken together, these studies suggest that age-associated loss of the ability to generate protective humoral immunity results in part from reduced B lymphopoiesis. As the output of new, naïve B cells declines, homeostatic pressures presumably force the filling of the peripheral B cell pool by long-lived antigen-experienced cells. Because the antibody repertoire of these cells is restricted by previous antigenic experience, they make poor quality responses to new immunologic insults. BioMed Central 2004 2004-05-10 /pmc/articles/PMC464870/ /pubmed/15225355 http://dx.doi.org/10.1186/ar1180 Text en Copyright © 2004 BioMed Central Ltd
spellingShingle Review
Johnson, Sara A
Cambier, John C
Ageing, autoimmunity and arthritis: Senescence of the B cell compartment – implications for humoral immunity
title Ageing, autoimmunity and arthritis: Senescence of the B cell compartment – implications for humoral immunity
title_full Ageing, autoimmunity and arthritis: Senescence of the B cell compartment – implications for humoral immunity
title_fullStr Ageing, autoimmunity and arthritis: Senescence of the B cell compartment – implications for humoral immunity
title_full_unstemmed Ageing, autoimmunity and arthritis: Senescence of the B cell compartment – implications for humoral immunity
title_short Ageing, autoimmunity and arthritis: Senescence of the B cell compartment – implications for humoral immunity
title_sort ageing, autoimmunity and arthritis: senescence of the b cell compartment – implications for humoral immunity
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC464870/
https://www.ncbi.nlm.nih.gov/pubmed/15225355
http://dx.doi.org/10.1186/ar1180
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