In immunology, a memory B cell (MBC) is a sort of B lymphocyte that kinds 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 perform is to memorize the traits of the antigen that activated their mum or dad B cell throughout preliminary infection such that if the memory B cell later encounters the same antigen, it triggers an accelerated and strong secondary immune response. Memory B cells have B cell receptors (BCRs) on their cell membrane, equivalent to the one on their dad or mum cell, that allow them to acknowledge antigen and mount a particular antibody response. In a T-cell dependent improvement pathway, naïve follicular B cells are activated by antigen-presenting follicular B helper T cells (TFH) throughout the preliminary infection, or primary immune response. B cells could even be activated by binding international antigen within the periphery where they then transfer 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 sting of the follicle bordering the T cell area. The B cells internalize the foreign peptides, break them down, and specific them on class II main histocompatibility complexes (MHCII), that are cell surface proteins. Within the secondary lymphoid organs, a lot of the B cells will enter B-cell follicles the place a germinal middle will form. Most B cells will eventually differentiate into plasma cells or memory B cells throughout the germinal center. The TFHs that categorical T cell receptors (TCRs) cognate to the peptide (i.e. particular for the peptide-MHCII advanced) on the border of the B cell follicle and T-cell zone will bind to the MHCII ligand. The T cells will then specific the CD40 ligand (CD40L) molecule and will begin to secrete cytokines which trigger the B cells to proliferate and to endure class switch recombination, a mutation in the B cell's genetic coding that modifications their immunoglobulin type.

Class switching allows memory B cells to secrete various kinds of antibodies in future immune responses. The B cells then either differentiate into plasma cells, germinal center B cells, or memory B cells depending on the expressed transcription elements. The activated B cells that expressed the transcription factor Bcl-6 will enter B-cell follicles and undergo germinal heart reactions. Once contained in the germinal heart, the B cells undergo proliferation, adopted by mutation of the genetic coding region of their BCR, a process often known as somatic hypermutation. The mutations will either improve or lower the affinity of the surface receptor for a specific antigen, a progression called affinity maturation. After buying these mutations, the receptors on the surface of the B cells (B cell receptors) are examined throughout the germinal heart for his or her affinity to the present antigen. B cell clones with mutations that have elevated the affinity of their floor receptors receive survival indicators through interactions with their cognate TFH cells. The B cells that would not have excessive sufficient affinity to receive these survival alerts, in addition to B cells which might be potentially auto-reactive, can be selected in opposition to and die through apoptosis.

These processes improve variability at the antigen binding sites such that every newly generated B cell has a novel receptor. After differentiation, memory B cells relocate to the periphery of the physique where they will be extra prone to encounter antigen in the event of a future publicity. Lots of the circulating B cells turn into concentrated in areas of the body that have a high likelihood of coming into contact with antigen, such as the Peyer's patch. The means of differentiation into Memory Wave Experience B cells inside the germinal heart is not yet totally understood. Some researchers hypothesize that differentiation into memory B cells occurs randomly. Other hypotheses propose that the transcription factor NF-κB and the cytokine IL-24 are involved in the strategy of differentiation into memory B cells. An additional hypothesis states that the B cells with comparatively decrease affinity for antigen will turn into Memory Wave B cells, in contrast to B cells with comparatively higher affinity that will develop into plasma cells.