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B cell activation occurs in the secondary lymphoid organs (SLOs), such as the spleen and lymph nodes. [1] After B cells mature in the bone marrow, they migrate through the blood to SLOs, which receive a constant supply of antigen through circulating lymph. [14] At the SLO, B cell activation begins when the B cell binds to an antigen via its BCR ...
Positive selection is based on steady cross-talk between T FH cells and their cognate antigen presenting GC B cell. Because a limited number of T FH cells reside in the germinal center, only highly competitive B cells stably conjugate with T FH cells and thus receive T cell-dependent survival signals. B cell progeny that have undergone SHM, but ...
Most textbooks say that B Cells mature in the bone marrow but, generally, immature B cells migrate to the spleen for 'higher education' of some sort where they go through transitional stages before final maturation. (Medical Immunology, p. 136) B lymphocytes are identified by the presence of soluble immunoglobulin G (IgG). This is the most ...
Germinal centers or germinal centres (GCs) are transiently formed structures within B cell zone (follicles) in secondary lymphoid organs – lymph nodes, ileal Peyer's patches, and the spleen [1] – where mature B cells are activated, proliferate, differentiate, and mutate their antibody genes (through somatic hypermutation aimed at achieving higher affinity) during a normal immune response ...
Transitional B cells that survive selection against autoreactivity develop eventually into naive B cells. [3] Given the fact that only a small fraction of immature B cells survive the transition to the mature naive stage, the transitional B cell compartment is widely believed to represent a key negative selection checkpoint for autoreactive B ...
A cell may stay in this state for several days, and then either die or irrevocably differentiate into a mature, fully differentiated plasma cell. [12] Differentiation of mature B cells into plasma cells is dependent upon the transcription factors Blimp-1/PRDM1, BCL6, and IRF4. [10]
Somatic hypermutation (or SHM) is a cellular mechanism by which the immune system adapts to the new foreign elements that confront it (e.g. microbes).A major component of the process of affinity maturation, SHM diversifies B cell receptors used to recognize foreign elements and allows the immune system to adapt its response to new threats during the lifetime of an organism. [1]
Later, difficulties with the subject B cell populations began to emerge, as there wasn't yet a stable long-term method of culture or isolation of individual subtypes. The difficulty of obtaining populations of viable B cell precursors was resolved by the design of a long-term bone marrow culture system, which secreted LP1 growth factor. [5]