The immune system is a complex defense mechanism the body develops to fight and destroy the infectious microorganisms or pathogens. The system consists of cells called lymphocytes, which are divided into two types: B-cells and T-cells. These lymphocytes are produced by the heamtpoietic stem cells found in the bone marrow (1).
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This essay discusses the B-cells that are involved in the humoral immune response. It also discusses the role of B-cells in the immune system, antibody production mechanism, and a disease associated with the malfunction of the B – cell mechanism.
The humoral immune response is one of the two main types of the immune system. This response occurs when the immune system triggers specific B-cells to proliferate and secrete specific antibodies into the bloodstream. As a result, these antibodies “patrol” the body and destroy the pathogens and thus prevent an infection. In essence, the antibodies produced have different affinities for various antigens.
Therefore, prior to antigen exposure, each B-Cell secretes a unique antibody on its surface that enables the immune system to respond appropriately to a variety of microorganisms that could possibly attack the body (1).
Antibodies belong to a family of immunoglobulin proteins (Ig), and they share some common features. For instance, all antibodies consist of four polypeptide chains made up of two light and two heavy chains joined together by disulfide bridges (1). In addition, they consist of two regions: the constant region that is next the C-terminal and the variable region adjacent to the N-terminal. These two regions results in the production of a variety of antibodies (1).
The variable region is caused by VDJ recombination, somatic hypermutation, and class switching. Basically, VDJ recombination occurs in the bone marrow and it is activated by the recombination activating genes proteins 1and 2 (RAG-1/2). The RAG-1/2 causes double strand breaking in the DNA during the recombination signal sequences (RSS) flanking the variable domains (1).
Therefore, immediately the DNA strand breaking occurs, the genes get shuffled giving rise to a variety of antibodies (1). On the other hand, somatic hypermutation involves the production of mutations, such as point mutations, substitution, duplications, or deletions in the DNA variable coding regions (1). Finally, class switching occurs in mature B-cells and it involves the replacement of the heavy chain constant regions.
Antibody production by B-cells follows a specific mechanism hypothesized by the clonal selection theory (1). The theory provides that each B-cell follows a specific lineage in producing unique antibodies. This allows the cells to identify a pathogen in the body only when specific antibodies on its surface bind with the corresponding antigens. The binding activates the B-cell receptors (BCR) resulting in a series of phophorylation reactions by the protein tyrosine kinases (PTK).
This induces the release of intracellular calcium ions needed for B-cell activation. Consequently, the bound antigen is engulfed by the B-cell causing it to undergo proteolysis, and the fragments produced are displayed on its surface by the cell surface molecule major histocompatibilty complex (MHC) II (1).
The antigen/MHC complex attracts the matching helper T-cell, which secretes lymphokines enzymes to activate the B-Cell (1). Therefore, an active B-cell begins to proliferate while producing plasma cells that secrete large quantities of antibodies into the blood stream. Thus, the antibodies released circulate in the blood and lymph vessels to identify and destroy the pathogens.
X-linked agammaglobulinemia (XLA) disorder is caused by a mutation in the Bruton tyrosine kinase (BTK) gene (2). Normally, the BTK gene causes the release of intracellular calcium ions needed for B-cell activation when the BCR is activated (2). Therefore, individuals suffering from this disorder develop a weaker immune system, and are susceptible to recurrent bacterial infections (3).
Currently, the treatment available for XLA patients is the lifelong antibody replacement therapy (3). However, an alternative therapy involving a lentiviral vector (LV) containing the immunoglobulin enhancer and IgB, is being tested on the mice without BTK genes.
In conclusion, appropriate knowledge about B-cells function and antibody production mechanisms is crucial in the medical field. This will ensure that the treatment of various diseases associated with B-cells is improved. B-cells represent just a section of the immune response against pathogens as the real immune system is complex and involves more that the humoral response.