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[Prev] | [Next]Lymphocytes are the other major type of white blood cells important in the immune system, and they work in concert with phagocytic cells to combat infections. However, the role lymphocytes play in fighting infections is very different than that played by phagocytes. Lymphocytes, with the help of antigen-presenting cells, are part of what is called the adaptive immune system. This system has three important features that all depend on lymphocytes.
B lymphocytes or B cells are the class of immune cells that synthesize antibodies and are responsible for humoral or antibody-mediated immunity. Antibodies react with antigens and the immune system has a virtually unlimited capacity to create antibodies that react with millions of potential antigens.
Each B cell contains on its surface about 100,000 antibody molecules (IgD or IgM) The binding sites of these antibodies are identical so that they all react specifically to the same antigenic structure, but they are different from the surface antibodies on other B cells. These membrane-bound antibodies serve as receptors for the antigen and contain two additional polypeptides (dimers of a protein called Ig-α/Ig-β) that span the cellular membrane and play a role in transmitting the binding of antigen to antibody to the cytoplasm of the cell as shown in Figure 15-15. Binding of an antigen by several different antibody receptors on the surface of the cell causes the receptors to cluster in a small area. This clumping of membrane bound antibody molecules then activates a signaling cascade that eventually results in the transcription of genes and thus the production of proteins important for B cell activation.
Binding of antibody activates tyrosine kinase and tyrosine phosphorylase in the cytoplasm that then phosphorylates and dephosphorylates tyrosine residues on the Ig-α/Ig-β polypeptide. These phosphorylation/dephosphorylation reactions activate B cells by at least three different pathways: (i) Activated tyrosine residues on the Ig-α/Ig-β polypeptide cause phospholipase C activity to increase. Phospholipase C then cleaves phospholipids into inositol triphosphate and diacyl glycerol. Diacyl glycerol activates protein kinase C eventually leading to the formation of nuclear factor NF-κB. (ii) Inositol triphosphate causes Ca2+ influx from the endoplasmic reticulum and the outside environment. Increased Ca2+ concentrations activate calmodulin that in turn phosphorylates Ets-1, a DNA binding protein. (iii) Activated tyrosine residues on the Ig-α/Ig-β polypeptide activate the p21ras protein, which leads to the activation of a serine/threonine kinase. This in turn phosphorylates cJUN, another DNA binding protein. NF-κB, Ets-1 and cJUN then travel to the nucleus and cause the transcription of specific genes important in B cell activation.
The activated B cell then goes through a process of rapid division (termed clonal expansion) where many more copies of the cell are made. Some of these cells differentiate into plasma cells that produce large amounts of antibody. The antibody molecules produced specifically react with the antigen that caused the initial activation of the B cell. A fraction of the cells from the clonal expansion remain as undifferentiated B memory cells that are capable of reacting with a second antigen challenge at a later time. If a future challenge does appear, this secondary response is much more rapid, normally inactivating the pathogen before a detectable infection appears.
The "B" of B cell comes from the Bursa of Fabricius, where B cells differentiate in birds. (Some of the early research on the immune system was done in chickens). In mammals, B cells mature in the bone marrow and MALT (especially MALT in the intestines) and then travel in the bloodstream eventually settling in immune tissues throughout the body with high concentrations in the lymph nodes and spleen.
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