Johnson Sara A, Cambier John C
Integrated Department of Immunology, University of Colorado Health Sciences Center and National Jewish Medical and Research Center, Denver, Colorado, USA.
Arthritis Res Ther. 2004;6(4):131-9. doi: 10.1186/ar1180. Epub 2004 May 10.
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.
免疫衰老与T和B淋巴细胞功能的衰退相关。尽管老年个体外周血中B细胞数量正常,且能够产生强烈的体液免疫反应,但所产生的抗体亲和力通常较低,且保护性不如年轻动物产生的抗体。在此,我们综述了多项探讨导致这种衰退机制的研究。综合来看,这些研究表明,与年龄相关的产生保护性体液免疫能力的丧失部分是由于B淋巴细胞生成减少所致。随着新生未成熟B细胞的输出减少,稳态压力可能迫使外周B细胞库由长寿的抗原接触过的细胞填充。由于这些细胞的抗体库受到先前抗原接触经历的限制,它们对新的免疫刺激产生的反应质量较差。