Came across this article and wanted to share it with you all.
greenmedinfo.com/blog/genet...
The following passage may have a clue as to why Auto Immune Disorders occur.
Some proteins that cells synthesize have awesome capabilities that can lead to great mischief if they get corrupted. Two of these are activation induced deaminase (AID) and nucleoprotein 98 (Nup98). Under cellular conditions of systemic extreme hyperphosphorylation, these two proteins collaborate to drive a cell into a cancerous state. Phosphorylation is an intriguing mechanism by which cells can modify their proteins and change their behavior, and it involves attaching a phosphate anion to either a serine or a threonine residue within the protein. Some proteins are profoundly affected by such a change, in some cases activated and in other cases inactivated by this small perturbation of the protein’s structure [44].
AID (not to be confused with AIDS!) was only first discovered in 1998, but the number of papers published on AID has been growing exponentially ever since. More and more of its roles in the body are being revealed over time, as well as its ability to cause harm if its expression is misregulated. AID’s specific action is to deaminate a cytosine nucleotide in a DNA molecule. This simple modification can lead to a double-strand break, which is then aggressively repaired by a suite of specialized DNA repair enzymes. However, these enzymes can make a mistake during the repair process, ending up with a DNA mutation, or even a wholesale rearrangement of a chromosome if the wrong ends get sewn together.
AID plays an essential role in the immune system, first, by launching the processes, called somatic hypermutation and class switch recombination, by which specific immunoglobulins in immature immune cells are modified within the thymus during infancy [45]. These raw immunoglobulin templates are eventually converted into an enormous number of variants that can later serve as antibodies to foreign antigens. Later on, at a time when a particular antigen, for example, from an invasive virus, presents itself, AID again becomes active to perfect the shape of the antibody so that it will be able to perfectly recognize and tag the viruses, making them readily visible to other immune cells that will then clear (phagocytose) them. If AID is dysfunctional, these processes will become imperfect, and the immune cells will not be able to optimize the shape of the antibodies. They can potentially end up tagging native proteins rather than foreign proteins, in a pathological process called molecular mimicry, leading to both autoimmune disease and immune deficiency.
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