As effective as the body’s own defense mechanisms usually are, it is dangerous when the regulatory mechanisms fail and the immune system turns against the body’s own tissue. Important members of the defense force are the T cells, which were trained in childhood and adolescence in the thymus to check and recognize the body’s own MHC identity papers.
How does immune deficiency disease develop?
For reasons that have not yet been definitively explained, these T cells can become saboteurs: Instead of attacking foreign invaders, they pounce on body tissue and destroy its cells. In the process, they attract other defense cells to their side, so that the body’s own structures are treated like antigens of foreign cells and are subsequently subjected to a massive attack.
The immunoglobulins directed against the body’s own tissue are also called autoantibodies (auto=self). The body’s repair squad does its best to repair the damage, but is at a loss – sooner or later the attacked organ is so destroyed that it loses its function.
Another consequence is that the immune system no longer has sufficient strength for its actual tasks due to its permanent attacks in the wrong place. Therefore, pathogens from the outside as well as cancer cells from the inside can spread and lead to corresponding diseases – thus, additional symptoms of an immune deficiency disease develop.
Hereditary and environmental factors
The cause is thought to be a combination of hereditary susceptibility and certain environmental factors, meaning that certain triggers, such as stress, pregnancy, or infections, only lead to autoimmune disease in those individuals who have a genetic predisposition to it.
It is still unclear exactly when and why the disease occurs. However, it is known that certain pathogens can also trigger an autoimmune disease, namely when their surface closely resembles the structure of the body’s own cells. If the immune system now forms antibodies against the germ, these also attack the body’s own similar tissue.
This is the case, for example, in rheumatic fever: antibodies against certain streptococci (e.g. scarlet fever pathogens) are later also directed against joint, kidney or heart muscle tissue. But this, too, probably only happens in people who have a hereditary predisposition.
Opinions are divided on the extent to which the psychological aspect plays a role not only in the management and course, but also in the development of the disease.
Consequential defect
In most cases, autoimmune diseases begin between the ages of 20 and 50. The specific symptoms that occur depend on which tissue is targeted by the autoimmune and inflammatory process. Currently, about 60 autoimmune diseases are known, which are either limited to certain organs (organ-specific) or manifest in the entire body (systemic), e.g. because they are directed against vessels, joints or connective tissue; both forms can occur in mixed form (intermediate).
Typical examples of affected tissues include:
- Organ-specific autoimmune diseases: Diabetes mellitus type 1 (pancreas), multiple sclerosis (neurons), glomerulonephritis (kidney), Hashimoto’s thyroidits (thyroid), Graves’ disease (thyroid), chronic gastritis (stomach), ulcerative colitis (colon), vitiligo (skin), Addison’s disease (adrenal glands).
- Systemic autoimmune diseases: Churg-Strauss syndrome (vessels), collagenoses (connective tissue), rheumatoid arthritis (connective tissue of joints and tendons), psoriasis (skin, joints, fingernails).
Diagnosis is made mainly by determining the antibodies in the blood – which are examined depends on the symptoms and the suspected diagnosis.
