As we all well know, the adaptive component of the immune system deteriorates with age for a number of reasons. There is the toll of cell and tissue damage, there is a structural issue in which too many cells become uselessly devoted to persistent viral infections and can no longer respond to new pathogens, there is inflammaging, in which the immune system is constantly overactive, producing chronic inflammation to no good end, and there is the atrophy of the thymus where T cells mature, which greatly reduces the pace at which new T cells are generated. B cells, however, do not mature in the thymus, and here researchers provide evidence to suggest that the B cell population of the active immune system doesn't meaningfully age for much of life in our species. They didn't look at everything, however, and you might compare this open access paper with evidence from past years of a decline in B cell function.
We analysed the genome-wide expression profiles of naive and whole B cell populations from young and early aged healthy donors under 60 years. We revealed large homogeneity of all analysed genome-wide expression profiles but did not identify any significant gene deregulation between young (30-45 years) and early aged healthy donors (50-60 years). We argue that B cells avoid the aging program on molecular level until 60 years of age.
Genome-wide analyses have detection limits, which in turn could limit identification of age-specific genes. Only minor gene alteration might be hidden below the detection threshold and unrecognized in this study. Nevertheless, our genome-wide analysis homogeneity indicated result robustness and confident reliability. We summarize surprising observations that human B lymphocytes remain almost identical at the molecular level during 30 to 60 years of age. As the immune system declines, the predispositions to B cell lineage malignancy manifested in some individuals below 60 years of age could not be addressed to natural healthy aging of B lymphocytes. Rather, other aspects might be involved including compromised body environment, declined cell stimulation, immune cell population disorders, clonal accumulations, infection history, life style and other individual behaviour contributing to early onset of aging.
The molecular identity of young and early aged B cells demonstrated potential of hematopoietic stem cells to generate uncompromised progenitor lymphocytes, naive and mature B cells in early elderly. These are very encouraging findings for general health, because the immunity maintenance does not seems to needed artificial intervention to keep B cells uncompromised in the early elderly.