Humoral immunity is also called antibody-mediated immunity. With assistance from helper T cells, B cells will differentiate into plasma B cells that can produce antibodies against a specific antigen. The humoral immune system deals with antigens from pathogens that are freely circulating, or outside the infected cells. Antibodies produced by the B cells will bind to antigens, neutralizing them, or causing lysis (dissolution or destruction of cells by a lysin) or phagocytosis. It is a function of B cells.
Types of Humoral Immunity
Humoral immunity can be subdivided into active and passive immunity. In active immunity the person actively makes an antibody after exposure to a foreign antigen. Active immunity can be artificial (e.g., following vaccination with a live or attenuated virus), or natural (e.g., following exposure to a disease-causing organism). In passive immunity a person is given an antibody that has been made by someone else. It can be artificial (e.g., gamma globulin given to people with agammaglobulinemia) or natural (e.g., maternal antibody that has crossed the placenta into the fetus).
Humoral immune deficiencies are conditions which cause impairment of humoral immunity, which can lead to immunodeficiency. It can be mediated by insufficient number or function of B cells, the plasma cells they differentiate into, or the antibody secreted by the plasma cells.
B cell activation: When a B cell encounters an antigen, the antigen is bound to the receptor and taken inside the B cell by endocytosis. The antigen is processed and presented on the B cell's surface again by MHC-II proteins.
B cell proliferation: The B cell waits for a helper T cell (TH) to bind to the complex. This binding will activate the TH cell, which then releases cytokines that induce B cells to divide rapidly, making thousands of identical clones of the B cell. These daughter cells either become plasma cells or memory cells. The memory B cells remain inactive here; later when these memory B cells encounter the same antigen due to reinfection, they divide and form plasma cells. On the other hand, the plasma cells produce a large number of antibodies which are released free into the circulatory system.
Now these antibodies will encounter antigens and bind with them. This will either interfere with the chemical interaction between host and foreign cells, or they may form bridges between their antigenic sites hindering their proper functioning, or their presence will attract macrophages or killer cells to attack and phagocytose them.
Example: Innate immunity also comes in a protein chemical form, called innate humoral immunity. Examples include the body's complement system and substances called interferon and interleukin-1 (which causes fever). Immune serum globulin (given for hepatitis exposure) and tetanus antitoxin are examples of passive immunization. Young individuals found to have ANA are more likely to have associated illnesses, such as systemic lupus erythematosus, compared with older individuals with the same level of ANA.
Overall, the humoral immune system plays a role in the initiation and regulation of the inflammatory response and elimination of pathogens. Further research is needed to determine the mechanisms of action and interactions of multiple components of humoral immunity, as well as their role in the pathogenesis of infection, neoplasia, and atherosclerosis.
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