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Autoimmune Diseases

The immune system is a critical component for human survival. Without the immune system, the human body would be vulnerable to invading microorganisms such as viruses and bacteria. However, an aberrant immune response may trigger the destruction of self-antigens, leading to a condition called Autoimmune Diseases. The autoimmune response involves both T-cells and B-cells. T-cells contain T-Cell Receptors (TCR) that can detect and destroy foreign antigens. Some TCRs can detect self-antigens but are destroyed by the thymic epithelial cells. However, some T-cells escape the thymic selection and instruct the B cells to make antibodies against self-antigens. The production of autoantibodies results in increased inflammation and tissue and organ damage leading to autoimmune diseases.

Mechanism: 

There are various mechanisms by which autoimmune diseases can occur. They are as follows:

  • Escape of helper T-cell tolerance: Helper T-cells (Th) are critical for normal immune response. If the tolerance to T-cells is bypassed or substituted, it may lead to the manifestation of autoimmune diseases.
  • Release of hidden or sequestered antigens: Some self-antigens may undergo sequestration during development (for example, spermatozoa, myelin basic protein) and, if released into circulation, may be identified as foreign and can mount an autoimmune response.
  • Functional imbalance of suppressor helper T-cells: Loss or excessive function of Th cells may also contribute to an autoimmune response
  • Molecular mimicry: Certain microorganisms may have antigens that resemble host antigens and thereby may cross-react with the host tissue and mount an autoimmune response.
  • Polyclonal activation of lymphocytes: Multiple microorganisms and their products (for example, bacterial Lipopolysaccharides (LPS)) are capable of inducing polyclonal activation of B-cells leading to the production of autoantibodies.

Classification:

Depending on the pathogenic mechanism, autoimmune diseases are classified into 2 types:

A. Organ-specific (auto-response directed against one organ) autoimmune disease

B. Systematic (auto-response directed against an antigen located on different sites of several organs or tissues) autoimmune disease

Manifestation:

Autoimmune diseases may manifest by a combination of factors such as genetics and environmental factors such as infections, toxins, hormones, microbiome, and tissue injury. Most autoimmune diseases are polygenic, which means more than one gene is involved in the disease. Additionally, patients who have a history of autoimmune disease may play a significant role. Finally, mutations in genes that regulate inflammation may make the individual susceptible to autoimmune diseases.

There are three main sets of genes that are known to play a critical role in autoimmune diseases: Immunoglobulins, T-Cell Receptors (TCR), and Major Histocompatibility complexes (MHC). With regards to the environment, several studies have demonstrated that environmental agents such as toxins, microbial infections, UV radiations, hormones, etc. contribute to the pathogenesis of autoimmune diseases.    


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