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Immunoglobulins are antibodies, a family of proteins and have two main functions. First one is to recognise and bind to antigen which is a foreign material. They bind to molecular structures on the surface of the antigens i.e. antigenic determinants which differ from the molecular structures made by the cell of the host. Second one is deployed to trigger elimination of foreign material. This involves binding of effector molecules to antibody coated foreign material to trigger complex elimination mechanisms e.g. the complement system of proteins, phagocytosis by host immune cells such as neutrophils and macrophages (Delves et al, 2009).
There are five distinct classes of immunoglobulins namely IgG, IgA, IgM, IgD and IgE. Each Immunoglobulin molecule is bifunctional where one region of the molecule is concerned with binding to antigen while a different region mediates effector functions which include binding of the immunoglobulins to host tissues, various cells of the immune system, to some phagocytic cells and to the first component of the classical component system (Roitt, Brostoff and Male, 2001).
The five classes have distinct functions. IgG has four subclasses IgG1, IgG2, IgG3 and IgG4 which account for approximately 70%, 19%, 18% and 3% respectively of the total IgG protein. IgG is produced as a result of the secondary immune response and is the only immunoglobulin that is transferred through the placenta to provide the neonate with some protection. All IgG subclasses except IgG4 can bind to C1q to activate complement. IgG can also act as an opsonin by cross linking immune complexes to Fc receptors on neutrophils and macrophages (Zubay, 1998). IgA accounts for 15% of total antibody found in serum and is the primary antibody found in exocrine excretions, saliva, tears and nasal secretions (Brostoff et al, 1991). IgM accounts for 5%-10% of serum antibody and is produced rapidly after exposure to an antigen and accounts for the primary immune response with production lasting only a few weeks. It is also very efficient at fixing complement (Roitt, Brostoff and Male, 1998). IgD accounts for less than 1% of serum antibody and thus it is a trace antibody and is usually cell membrane bound on B cells co-expressed with IgM. It is less stable than IgG as it is subject to proteolysis (Roitt, Brostoff and Male). IgE binds with high and low affinity Fc receptors found on mast cells and basophils or leukocytes and lymphocytes respectively and is produces in response to parasitaemia. IgE binding to Fc receptors on mast cells stimulates histamine release and thus hypersensitivity reactions like asthma and hay fever (Roitt, Brostoff and Male, 1998).
An immune response has 2 phases which include the recognition of antigen and a reaction to eradicate it (Roitt, Brostoff and Male, 1998). Acquired immunity has two branches the humoral and cell mediated. Humoral is antibody mediated and the functions of antibodies in providing these are the recognition of antigen which is done through the receptors present on surfaces of B lymphocytes, Neutralisation of antigen, activation of complement and Opsonisation. Humoral immune response is the principal defence mechanism against extracellular microbes and their secreted toxins. B cells express surface immunoglobulin to bind with antigen (Hossain A, 2003).
At various times in the immune response there are qualitative and quantitative differences in antibody production. The first response is the primary response consisting of the lag phase which includes the time elapsed after initial contact with an antigen before antibody is detected in serum. The latent period includes the time taken for B cells to make contact with the antigen, proliferate, differentiate and secrete antibodies in sufficient quantity to be detected in serum, Log phase in which the concentration of antibodies in serum increases exponentially, Plateau phase in which a constant antibody level is maintained and decline phase in which serum antibody levels decline due to clearing to antigen-antibody complexes and natural catabolism of immunoglobulins. The second response is the secondary response and here the lag phase is much shorter than in the primary response while the plateau and decline phases are extended. During this response there is marked change in both quantitative and qualitative production of antibody e.g. affinity maturation where there is a change in amino acid sequence of antibody polypeptide to make them more capable of binding antigen. There is also a shift in the isotype response (Hossain A, 2003).
In the primary response there is considerable lag phase before antibody can be detected in serum. B cells are stimulated and they produce IgM. Isotype class switching occurs leading to production of other antibodies like IgG and IgE. Equilibrium is reached when there is balance between antibody production and utilisation and the response will die out when no longer needed. In secondary response, the responding cells are present in increased number and at different levels of activation and differentiation thus a shorter lag phase. The main isotype is IgG since the memory cells generated in primary response have undergone class switching from IgM to IgG.The level of antibody production is secondary response is 10 times more than in primary response and antibody is present for an extended period with greater affinity for antigen due to affinity maturation. Some IgM is also produced here and this is by activation of B cells that were not present in the lymphocytes pool at primary exposure but have developed after secondary exposure (Hossain A, 2003).
People with immunoglobulin deficiencies are prone to more frequent illness especially those caused by bacteria in particular the encapsulated ones because these capsules are not easily recognised by the defective immune system and also some viral infections, in particular those caused by echovirus, enterovirus, and hepatitis B. These deficiencies can be either primary or secondary disorders. A secondary deficiency results from some other ongoing ailment or treatment e.g. chemotherapy for cancer can compromise the immune system, leading to immunodeficiency and once treatment is stopped the immunodeficiency can be reversed. A primary immunodeficiency is as a result of a genetic disorder or a defect to B cells or other immune cells (bookrags, 2006). The most prevalent type of immunodeficiency disorders are listed below
X-linked agammaglobulinemia which is an inherited disease due to a defect on the X chromosome and this disease is seen more frequently in males than females. It results in a failure of B-cells to mature and thus they will not be capable to make antibodies and to develop "memory," in which the B-cell will rapidly recognize and respond to an infectious agent the next time it is encountered. All classes of antibodies are decreased in this condition.
Selective IgA deficiency is an inherited disorder as a result of failure of B-cells to switch class from IgM to IgA during early response and although the B-cell numbers are normal and can still make all other classes of antibodies but the amount of IgA produced is limited. This results in more infections of mucosal surfaces like the nose, throat, lungs, and intestines (Thefreedictionary, 2010).
Transient hypogammaglobulinemia of infancy is a temporary disease which has an unknown cause however, it is believed to be caused by a defect in the development of T-helper cells which recognize foreign antigens and activate T- and B-cells in an immune response. As the child grows, the number of T-helper cells becomes normal by itself. Hypogammaglobulinemia is characterized by low levels of antibodies in the blood and patients have decreased levels of antibodies IgG and IgM (Thefreedictionary, 2010).
Common variable immunodeficiency is a defect in both B cells and T-lymphocytes and results in almost a complete lack of antibodies in the blood (Thefreedictionary, 2010).
"Immunoglobulin heavy chain deletion is a genetic disease in which part of the antibody molecule is not produced and results in the loss of several antibody classes and subclasses, including most IgG antibodies and all IgA and IgE antibodies. The disease occurs because a part of the gene for the heavy chain has been lost" (Thefreedictionary, 2010).
Selective IgG subclass deficiencies are a group of genetic diseases in which some of the 4 subclasses of IgG are missing. As the B-cell matures, it can switch from one subclass to another which does not occur in these disorders because of a defect in maturation of the B-cells.
IgG deficiency with hyper-IgM is a disease that is due to a genetic mutation and results from the failure of B-cell to switch from making IgM to IgG resulting in an increase in amount of IgM and a decrease in the amount of IgG (Thefreedictionary, 2010).
Primary immunoglobulin deficiency syndromes occur rarely of which those that are X-linked occur more in males. Detection of the syndromes usually occurs in childhood however numbers of new cases of the specific syndromes are difficult to estimate because many deficiencies go undiagnosed. Among the syndromes for which incidence rates are available are IgA deficiency is 1 in 500-700, agammaglobulinemia is 1 in 50,000-100,000, severe combined immunodeficiency (SCID) is 1 in 100,000-500,000 and common variable immunodeficiency (CVID) is 1 in 50,000-200,000 (Answers.com, 2006).