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In secondary lymphoid tissues, germinal centers (GCs) are created after exposure to T-dependent antigens.
As a result of somatic hypermutation, B cells with higher antibody affinities are produced in GCs. These high-affinity B cells then preferentially develop into plasma cells, which reside in the bone marrow and provide long-lasting humoral protection.
The physiological and molecular basis for starting the shift from a GC B cell to a plasma cell has been newly illuminated by recent investigations. Here, we review recent developments in our knowledge of how the GC response regulates the production of plasma cells in order to produce long-lasting protective immunity and avoid damaging autoimmunity.
The terminally developed B lymphocytes known as plasma cells release antibodies on a regular basis. These antibodies can defend against infections, and the greatest clinical correlates of vaccine effectiveness are their amount and quality.
Therefore, the plasma cell lifespan plays a major role in determining the duration of humoral immunity. However, autoimmune disorders or multiple myeloma can result from a breakdown in plasma cell activity. The primary determinants of plasma cell longevity are food intake and metabolic processes that are not transcriptionally regulated.
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