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  Humoral immunity

Humoral immunity:

The humoral immune response starts with the identification of antigen. However the classification divides the cell mediated and humoral immunity with dissimilar cell types they do interact to bring an effectual immune response. Specific T-cells are stimulated to generate lymphokines which are accountable for the antigen-induced B-cells proliferation and differentiation.

This is used for the T depended antigens. Though a number of the macro antigenic molecules can straight stimulate the B cells directly. By a process of clonal selection specific B-cells are gets stimulated, the activated B-cell first builds up into a B-lymphoblast, becoming very much larger and shedding all surface immunoglobulin. This terminal differentiation stage is accountable for making of primarily IgM antibody throughout the primary immune response. Some newly differentiated B-cells remain like long-lived “memory cells” without secreting antibodies. On subsequent encounter with antigen, these cells respond very rapidly to generate large amounts of IgG, IgA or IgE antibody, producing the better secondary immune response.

Pathogen or foreign protein + Macrophage / dentritic cells  → processed antigen

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The initial differentiation step which finally leads to the mature B-cell includes DNA rearrangements in heavy chain variable (V) region also identical rearrangements in the light chain genes to synthesis immunoglobulin. Of course these stages are, initiated on encounter with antigen and activation through T-helper cell to secrete lymphokines. The activated B-cell first develops into a B-lymphoblast, turns into very much larger.

IgM antibody is created in the ‘primary immune response.’ Instead, these cells go through secondary DNA rearrangements to change the stable region and types IgG, IgA or IgE antibodies throughout secondary immune response. The suppressor T-cells suppresses the immune response one time a sufficient amount of antibody formed. Other way of suppression takes place by the produced antibody itself and termed as, “antigen blocking”. While high doses of antibody interact along with the entire antigen’s epitopes thus inhibits interactions with B-cell receptors.

 

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