In immunology, a memory B cell (MBC) is a type of B lymphocyte that forms part of the adaptive immune system. These cells develop within germinal centers of the secondary lymphoid organs. Memory B cells circulate in the blood stream in a quiescent state, sometimes for decades. Their function is to memorize the characteristics of the antigen that activated their parent B cell during initial infection such that if the memory B cell later encounters the same antigen, it triggers an accelerated and robust secondary immune response. Memory B cells have B cell receptors (BCRs) on their cell membrane, identical to the one on their parent cell, that allow them to recognize antigen and mount a specific antibody response.
In a T-cell dependent development pathway, naïve follicular B cells are activated by antigen presenting follicular B helper T cells (TFH) during the initial infection, or primary immune response. Naïve B cells circulate through follicles in secondary lymphoid organs (i.e. spleen and lymph nodes) where they can be activated by a floating foreign peptide brought in through the lymph or by antigen presented by antigen presenting cells (APCs) such as dendritic cells (DCs). B cells may also be activated by binding foreign antigen in the periphery where they then move into the secondary lymphoid organs. A signal transduced by the binding of the peptide to the B cell causes the cells to migrate to the edge of the follicle bordering the T cell area.
The B cells internalize the foreign peptides, break them down, and express them on class II major histocompatibility complexes (MHCII), which are cell surface proteins. Within the secondary lymphoid organs, most of the B cells will enter B-cell follicles where a germinal center will form. Most B cells will eventually differentiate into plasma cells or memory B cells within the germinal center. The TFHs that express T cell receptors (TCRs) cognate to the peptide (i.e. specific for the peptide-MHCII complex) at the border of the B cell follicle and T-cell zone will bind to the MHCII ligand.
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