![]() B cell clones with mutations that have increased the affinity of their surface receptors receive survival signals via interactions with their cognate T FH cells. After acquiring these mutations, the receptors on the surface of the B cells (B cell receptors) are tested within the germinal center for their affinity to the current antigen. The mutations will either increase or decrease the affinity of the surface receptor for a particular antigen, a progression called affinity maturation. Once inside the germinal center, the B cells undergo proliferation, followed by mutation of the genetic coding region of their BCR, a process known as somatic hypermutation. The activated B cells that expressed the transcription factor Bcl-6 will enter B-cell follicles and undergo germinal center reactions. ![]() The B cells then either differentiate into plasma cells, germinal center B cells, or memory B cells depending on the expressed transcription factors. Class switching allows memory B cells to secrete different types of antibodies in future immune responses. The T cells will then express the CD40 ligand (CD40L) molecule and will begin to secrete cytokines which cause the B cells to proliferate and to undergo class switch recombination, a mutation in the B cell's genetic coding that changes their immunoglobulin type. specific for the peptide-MHCII complex) at the border of the B cell follicle and T-cell zone will bind to the MHCII ligand. The T FHs that express T cell receptors (TCRs) cognate to the peptide (i.e. Most B cells will eventually differentiate into plasma cells or memory B cells within the germinal center. Within the secondary lymphoid organs, most of the B cells will enter B-cell follicles where a germinal center will form. 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. 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. ![]() B cells may also be activated by binding foreign antigen in the periphery where they then move into the secondary lymphoid organs. 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). Naïve B cells circulate through follicles in secondary lymphoid organs (i.e. In a T-cell dependent development pathway, naïve follicular B cells are activated by antigen presenting follicular B helper T cells (T FH) during the initial infection, or primary immune response. Development and activation T cell dependent mechanisms 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. 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 circulate in the blood stream in a quiescent state, sometimes for decades. These cells develop within germinal centers of the secondary lymphoid organs. In immunology, a memory B cell ( MBC) is a type of B lymphocyte that forms part of the adaptive immune system. They form memory cells that remember the same pathogen for faster antibody production in future infections. B lymphocytes are the cells of the immune system that make antibodies to invading pathogens like viruses.
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