ANTIBODY-MEDIATED IMMUNITY (AMI)

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Antibody-mediated immunity (AMI) also known as humoural immune response is an acquired or adaptive immunity that is generally mediated by immunoglobulins or antibodies and B lymphocytes. Humoural immune response mainly protects against extracellular bacteria, toxins and other extracellular foreign molecules or pathogens. The B cells are mainly responsible for the production of antibody-secreting plasma cells and memory B cells; and both the B lymphocytes and the immunoglobulins are the main components of the AMI. After their stimulation, the B cells proliferate and differentiate into antibody-producing plasma cells which produce immunoglobulins that specifically bind antigens.

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The memory B cells produced during this process of B cell proliferation and differentiation ensure that antibody production occurs at a much faster rate in future exposures to antigens i.e., if the host animal or human is attacked the second time by the same or a similar antigen or antigenic molecule. The interaction of B lymphocytes with pathogens or antigens is the main prerequisite for the proliferation and differentiation of B cells into plasma cells and memory B cells with a long lifespan than naïve B cells. The plasma cells secrete numerous antibodies (the main effectors of humoural immunity) during the activation of B cells; and the immunoglobulins secreted are generally the main effector molecules of AMI. Immunoglobulins continuously police the blood circulation in the body and they mark out or identify and neutralize trapped antigens in the process. Antibodies are the main effectors of humoural immunity.

The coating of an antigen with antibody in vivo makes the foreign body to be easily attacked by other components of the immune system such as the engulfing of bacteria by phagocytes. The process of viral neutralization, opsonization, complement activation and phagocytosis are facilitated during immunological response when antigens are complexed with immunoglobulin molecules. The presence of immunoglobulins on mucosal surfaces including the GIT or intestinal tract, respiratory tract and nasal tract to mention but a few provides immunity to many infectious agents inclusive of pathogenic bacteria and viruses.

Deficiencies in the humoural immune response of a host may result in several microbial infections such as pyogenic infections that are bacterial-mediated i.e., caused by pathogenic bacteria. IgM is the first antibody to be produced during primary immune response – which is mainly characterized by the production of Ig-secreting plasma cells and memory B cells from the first contact of the host with exogenous antigens (Figure 1). In primary immune response, immunoglobulin production is slow. Naïve or incompetent B cells (that have not encountered a pathogen or antigen) undergo clonal selection after interacting with antigens to form antibody-secreting plasma cells and memory B cells. This phase of immune response (i.e., the primary immune response) is generally characterized by the initial production of numerous IgM which is later followed by the production of IgG. Primary immune response is a slower type of immune response which can last for a short time depending on the duration the invading antigen last in the host.

Figure 1. Schematic illustration of primary immune response. Photo courtesy: https://courses.lumenlearning.com/microbiology/chapter/overview-of-specific-adaptive-immunity/

In secondary immune response numerous amount of IgG is produced (Figure 2). Humoural immunity is generally responsible for providing defense against bacterial pathogens.  Secondary immune response occurs weeks, months or years later following the exposure of the individual to the same antigen that invaded the body previously.

Figure 2. Schematic illustration of secondary immune response. Photo courtesy: https://www.abpischools.org.uk/topic/pathogens/10       

Antibody production at this stage is mainly mediated by the memory B cells formed during the primary immune response. The memory B cells undergo a rapid proliferation and differentiation into immunoglobulin-secreting plasma cells that ensures that enormous amount of antibodies (particularly IgG) is produced against the invading pathogen or antigen. The amount of IgM produced in secondary immune response is usually lower when compared to the amount of IgM produced in primary immune response. And the high amount of IgG produced in secondary immune response ensures that immunological response occurs at a much faster rate than the slower reaction obtainable in the primary immune response.

Further reading

William E.P (2003). Fundamental Immunology. 5th edition. Lippincott Williams and Wilkins Publishers, USA.

Stevens, Christine Dorresteyn (2010). Clinical immunology and serology. Third edition. F.A. Davis Company, Philadelphia.

Silverstein A.M (1999). The history of immunology. In Paul, WE (ed): Fundamental Immunology, 4th edition. Lippincott Williams and Wilkins, Philadelphia, USA.

Paul W.E (2014). Fundamental Immunology. Seventh edition. Lippincott Williams and Wilkins, USA.

Male D, Brostoff J, Roth D.B and Roitt I (2014). Immunology. Eight edition. Elsevier Saunders, USA.

Levinson W (2010). Review of Medical Microbiology and Immunology. Twelfth edition. The McGraw-Hill Companies, USA. Berzofsky J.A and Berkower J.J (1999). Immunogenicity and antigen structure. In Fundamental Immunology, 4th edition., W.E. Paul, ed., Lippincott-Raven, Philadelphia. 

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