Written by MicroDok

Antibody-mediated immunity (AMI) also known as humoral immune response is an acquired or adaptive immunity that is generally mediated by immunoglobulins or antibodies and B lymphocytes. Humoral immune response mainly protects against extracellular bacteria, toxins and other extracellular foreign molecules. 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 binds antigens; and the memory B cells produced during this process ensure that antibody production occurs at a much faster rate in future i.e. if the host animal is attacked the second time by 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 humoral 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.

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 bacteria and viruses; and deficiencies in the humoral 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 16). In secondary immune response numerous amount of IgG is produced (Figure 17); and humoral immunity is generally responsible for providing defense against bacterial pathogens.

Figure 16: Schematic illustration of primary immune response. In primary immune response, immunoglobulin production is slow. Naïve or incompetent B cells 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 17: Schematic illustration of secondary immune response. Secondary immune response occurs weeks, months or years later following the exposure of the individual to the same antigen that invaded the body previously. Antibody production at this stage is mainly mediated by the memory B cells formed during the primary immune response; and 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.


Abbas A.K, Lichtman A.H and Pillai S (2010). Cellular and Molecular Immunology. Sixth edition. Saunders Elsevier Inc, USA.

Actor J (2014). Introductory Immunology. First edition. Academic Press, USA.

Alberts B, Bray D, Johnson A, Lewis J, Raff M, Roberts K and Walter P (1998). Essential Cell Biology: An Introduction to the Molecular Biology of the Cell. Third edition. Garland Publishing Inc., New York.

Bach F and Sachs D (1987). Transplantation immunology. N. Engl. J. Med. 317(8):402-409.

Barrett   J.T (1998).  Microbiology and Immunology Concepts.  Philadelphia,   PA:  Lippincott-Raven Publishers. USA.

Jaypal V (2007). Fundamentals of Medical Immunology. First edition. Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India.

John T.J and Samuel R (2000). Herd Immunity and Herd Effect: New Insights and Definitions. European Journal of Epidemiology, 16:601-606.

Levinson W (2010). Review of Medical Microbiology and Immunology. Twelfth edition. The McGraw-Hill Companies, USA.

Roitt I, Brostoff J and Male D (2001). Immunology. Sixth edition. Harcourt Publishers Limited, Spain.

Zon LI (1995). Developmental biology of hematopoiesis. Blood, 86(8): 2876–91.

About the author


Leave a Comment