Aspects of Response of the Immune System
There are several pathogens out there. How can you make antibodies to each particular pathogen? The answer is that antibody molecules go under several different mutations to produce higher affinities. CD4 helper cells recognize MHC II antigens. The somatic mutations that occur in the immunoglobulin gene also cause increased affinity. The joining regions of the VDJ of the antibody are the hot spots of the immunoglobulin in the final quest of the antibody to join with the antigen. There exist 10 to the 18th different possibilities due to the T-cell receptor J region variabilities as well. B-cells that don’t possess favorable variations become apoptotic (die off).
When oncogenes are mutated, the patients contracts cancer. This may the cause a vigorous T-cell response, in which the T-cells replicate exponentially. Most immunoglobulins are produced with the help of T-cells. In the absence of T-cells, the only immunoglobulin that can be manufactured is IgM. IgM doesn’t undergo somatic mutation. However, IgM still maintains regional binding affinity because it maintains up to ten binding sites. Subsequently, the antigen molecules must have a lot of binding sites as well for IgM to bind. So, the patient really needs IgG to bind to antigens with only one epitope. IgM does not get transported across the placenta. IgG molecules get transported across the placenta very well. Additionally, IgA molecules in a new mother’s milk has been shown to protect the new born from many infections. That’s why breast fed babies have considerably fewer infections than non breast fed babies. T-cells can’t recognize polysaccharides as antigens. Polysaccharides can’t get into MHC molecules.So, in the case of the tetanus vaccine, in which the tetanus toxoid is protected against, the immune system would be manufacturing IgM immunoglobulin. Most of the other mainstream vaccinations, protect against the micro-organisms causing the diseases.