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B cell activation: from immature B cell to plasma cell or memory B cell Basic B cell function: bind to an antigen, receive help from a cognate helper T cell, and differentiate into a plasma cell that secretes large numbers of antibodies. B cell activation occurs in the secondary lymphoid organs (SLOs), such as the spleen and lymph nodes. [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.
The latter case induces recognition by antigen-specific Th2 cells or Tfh cells, leading to activation of the B cell through binding of TCR to the MHC-antigen complex. It is followed by synthesis and presentation of CD40L (CD154) on the Th2 cell, which binds to CD40 on the B cell, thus the Th2 cell can co-stimulate the B cell. [11]
BLNK's function and importance in B cell development were first illustrated in BLNK deficient DT40 cells, a chicken B cell line. [7] DT40 cells had interrupted B cell development: there was no calcium mobilization response in the B cell, impaired activation of the mitogen-activated protein (MAP) kinases p38 , JNK , and somewhat inhibited ERK ...
In immunology, a naive B cell is a B cell that has not been exposed to an antigen. These are located in the tonsils , spleen , and primary lymphoid follicles in lymph nodes . Once exposed to an antigen , the naive B cell either becomes a memory B cell or a plasma cell that secretes antibodies specific to the antigen that was originally bound.
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]
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 .
CD32C is expressed in ~20% of the human population, and is not well-understood. [2] It can be found on B cells and natural killer (NK) cells. When expressed, CD32C plays an important role in the activation of antibody-dependent cell cytotoxicity (ADCC). [3] Animal studies have linked CD32C to augmentation of pathological inflammatory responses. [3]