Antibodies are important in the immunity against extracellular pathogens, but also against intracellular parasites, which spread through the extracellular space. They can support the immunity in three ways. Antibodies neutralize a pathogen which rely to intracellular metabolism or toxins and embarass them to enter the cell through the cell membrane via receptors.
Another important function of Antibodies is promoting the phagocytosis. This mechanism is called opsonization. The Phagocytes recognize the Fc region of an Antibody molecule which is bound on the surface of a pathogen.
The third capacity of antibodies is the activation of the complement system. Antibodies coating the surface of a pathogen can be recognized by the complement proteins which have different functions. Complement proteins can promote the phagocytosis or lysis of the pathogen.
Antibodies were produced by B cells. B cells are lymphocytes and belong to the adaptive immunity and emanate from the common lymphoid progenitors under the impact of IL-7. They undergo two different gene rearrangement (D-J and V-DJ rearrangement) before they express the B cell receptor (BCR) in the immature phase.
The BCR is specific to one epitope. If a epitope of a pathogen binds to the BCR, the B cell internalize and degrade them and bind the degraded particles to MHC II molecules. A CD4+ T-cell (Th2 cell response) binds to another epitope of the pathogen with the t cell receptor (TCR). The CD4 receptor binds coevally to the MHC II molecule. Both the MHC II:CD4 and the BCR:TCR signal and also the binding of CD40 to the CD40L are important for the activation of the T cell. This activation leads to the secretion of different cytokines from the T cell. IL-4, IL-5 and IL-6 leads to the proliferation and differentiation of the B cells.
The CD40:CD40L complex and different cytokine patterns leads also to an antigen class switch from IgM to IgG, IgE or IgA. After teh activation can the b cell differentiate to a plasma cell or to a memory b cell, which can produce faster and more IgG after a recurring infection.
[1] Murphy, K. et al. Janeway’s Immunobiology, 7th edition. Garland Science 2008
