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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 ...
Patients with XLA have normal pre-B cell populations in their bone marrow but these cells fail to mature and enter the circulation. The BTK gene is located on the X chromosome (Xq21.3-q22). [10] At least 400 mutations of the BTK gene have been identified. Of these, at least 212 are considered to be disease-causing mutations.
Mechanism of class-switch recombination that allows isotype switching in activated B cells. Immunoglobulin class switching, also known as isotype switching, isotypic commutation or class-switch recombination (CSR), is a biological mechanism that changes a B cell's production of immunoglobulin from one type to another, such as from the isotype IgM to the isotype IgG. [1]
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]
Cluster of Differentiation 86 (also known as CD86 and B7-2) is a protein constitutively expressed on dendritic cells, Langerhans cells, macrophages, B-cells (including memory B-cells), and on other antigen-presenting cells. [5] Along with CD80, CD86 provides costimulatory signals necessary for T cell activation and survival.
Activation of T cells without co-stimulation may lead to the unresponsiveness of the T cell (also called anergy), apoptosis or the acquisition of the immune tolerance. [ 3 ] The counterpart of the co-stimulatory signal is a (co-)inhibitory signal, where inhibitory molecules interact with different signaling pathways in order to arrest T cell ...
FCGR2B regulates B cell activation by increasing the BCR activation threshold and suppressing B cell-mediated antigen presentation to T cells through the ITIM-dependent inhibitory mechanism. [9] Ligation of FCGR2B on B cells downregulates antibody production, prevents the membrane organization of BCR and CD19 and promotes apoptosis .
The process of formation begins when the T-cell receptor binds to the peptide:MHC complex on the antigen-presenting cell and initiates signaling activation through formation of microclusters/lipid rafts. Specific signaling pathways lead to polarization of the T-cell by orienting its centrosome toward the site of the immunological synapse. The ...