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Aina Meducci 2012


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It is very hard to understand autoimmunity topic even though I have read for many times. As such, in medical perspective, autoimmune remain as mystery because the until now the researchers could not find the possible reason of why autoimmnune occurs.

Ps: Before read below post, make sure to understand basic immunity first!



Autoimmunity is the failure of an organism to recognize its own constituent parts as self, which allows an immune response against its own cells and tissues. Any disease that results from such an aberrant immune response is termed an autoimmune disease. Autoimmunity is often caused by a lack of germ development of a target body and as such the immune response acts against its own cells and tissues. Autoimmune diseases are very often treated with steroids.

It is also known as the failure of antibodies (B cells) or T cells to recognize own cell and launch attack against it.

Prominent examples include

  • Coeliac disease
  • diabetes mellitus type 1 (IDDM)
  • systemic lupus erythematosus (SLE)
  • Sj√∂gren's syndrome
  • Churg-Strauss Syndrome
  • Hashimoto's thyroiditis
  • Graves' disease,
  • idiopathic thrombocytopenic purpura
  • rheumatoid arthritis (RA)
  • lupus
  • allergies.
**Each of the disease has their own mechanism of autoimmune

Systemic lupus erythematosus

Grave disease

Rheumatoid disease

General Classification of autoimmunity

Autoimmune diseases are generally classified on the basis of the organ or tissue involved. These diseases may fall in an organ-specific category in which the immune response is directed against antigen(s) associated with the target organ being damaged or a non-organ-specific category in which the antibody is directed against an antigen not associated with the target organ

Causes of autoimmunity

The cause of autoimmune diseases is unknown, but it appears that there is an inherited predisposition in many cases. In a few types of autoimmune disease (such as rheumatic fever), a virus or infection with bacteria triggers an immune response and the antibodies or T-cells attack normal cells because some part of their structure resembles a part of the infecting microorganism.

Various theories have been offered. These include sequestered antigen, escape of auto-reactive clones, loss of suppressor cells, cross reactive antigens including exogenous antigens (pathogens) and altered self antigens (chemical and viral infections).

Sequestered antigen

Lymphoid cells may not be exposed to some self antigens during their differentiation, because they may be late-developing antigens or may be confined to specialized organs (e.g., testes, brain, eye, etc.). A release of antigens from these organs resulting from accidental traumatic injury or surgery can result in the stimulation of an immune response and initiation of an autoimmune disease.

Escape of auto-reactive clones

The negative selection in the thymus may not be fully functional to eliminate self reactive cells. Not all self antigens may be represented in the thymus or certain antigens may not be properly processed and presented.

Lack of regulatory T cells

There are fewer regulatory T-cells in many autoimmune diseases.

Cross reactive antigens

Antigens on certain pathogens may have determinants which cross react with self antigens and an immune response against these determinants may lead to effector cell or antibodies against tissue antigens. Post streptococcal nephritis and carditis, anticardiolipin antibodies during syphilis and association between Klebsiellaand ankylosing spondylitis are examples of such cross reactivity.


Normal vs autoimmune

Potential Immune Mechanism’s of Autoimmune Disease

Researchers don’t appear to have come to any definite conclusions regarding the mechanism’s of immune dysfunction behind autoimmune diseases. This is not surprising since the immune system itself is a new frontier of study.

The following are some examples of credible possibilities put forth by a variety of researchers. It’s an intricate area and experts don’t necessarily agree. There may also be some overlapping. Some theories are more widely held than others.

T Suppressor Cells

The function of T suppressor cells in the immune system is to stop the immune response; the foe is destroyed! T suppressor cells can “damp down” an immune response at the appropriate time.

It is a widely held belief that the seemingly unregulated autoantibody production in autoimmune disease is a result of inadequate T suppressor cell function. T suppressor cells also are thought to be responsible for distinguishing between “self” and foreign tissue and thus prevent autoimmunity.

“Decreased numbers and activity of T suppressor cells in patients with virtually all types of autoimmune disorders have been reported.” Drs. Isenberg and Morrow, Friendly Fire

T Helper Cells

The Helper T cell is the “quarterback” of the immune system. They’re the organizers of immune activity; aiding, abetting and directing virtually every facet of the immune system. Almost everything your immune system can do is dependent on the T Helper cell. It directs the activity
through the secretion of protein molecules called cytokines.

Interleukin 2 and Gamma Interferon are examples of cytokines. Cytokines are information molecules and are produced by other cells as well. T Helper cells produce Th1 and Th2 cytokine profiles, among others, based upon the cytokine environment (information/cytokines from other cells).

Th1 cytokines are great for promoting a defense against a viral or bacterial attack.Th2 cytokines organize defenses against parasites and mucosal infections but will shut down the activity of Th1 in the process. Some researchers believe that some viruses, bacteria and mycoplasma make proteins that mimic a cytokine that effectively turns on the Th2 cytokines thereby turning off the Th1 cytokines actually needed to promote killing them. This leaves the immune system, or part of it, in a state not fully functional for the task at hand.

Infection & Autoimmune

“There are intimate links between infectious agents (viruses, bacteria, etc) and autoimmunity.” Drs. Isenberg and Morrow

A similar perspective on infection is offered by Dr. Lauren Sompayrac, “For years physicians have noticed that autoimmune diseases frequently follow bacterial or viral infections, and immunologists believe that microbial attack may be one of the key environmental factors that trigger autoimmune disease.” Dr.Lauren Sompayrac, How the Immune System Works

The immune system is constantly being challenged by infection. Events can arise from infections if the immune system does not eliminate the invading organism quickly and efficiently.

Most researchers believe infection to be a trigger but also believe other conditions must be present. This is obvious since everyone who gets an infection does not get an autoimmune disease.

Molecular Mimicry

Another favored theory is that B cell and T cell receptors in the immune system recognize things that are similar as opposed to things identical. If a receptor is activated in the normal way by an invader, and “self” immune stimulators are present (in the same locality) at the same time, the immune system may react to both.

Another way of putting it is that some microorganisms trick the immune system into attacking “self” because of a superficial resemblance. Since the immune system has layers of tolerance or “self” protection, other break-downs in these systems are also required.

“Immunologists believe that the majority of autoimmune diseases result when the layers of tolerance inducing mechanisms fail to eliminate self-reactive cells in genetically normal individuals.” Dr. Lauren Sompayrac

Mechanisms Change

“Through the integrity of the immune system we remain separate from our environment. This inner image of ‘self-ness’ or uniqueness somehow carries through to each defensive cell as it works to eliminate cancer cells that arise daily or virus particles as they penetrate from the outside world.

The mechanisms by which this image of self is transmitted and carried out are still largely unknown. We do know that the mechanisms exist and, more important, that they are subject to change.

Macrophages, for example, do not merely mope about hoping to bump against a bacterium or other source of food. They migrate from distant corners of the body, zero in on targets that they ‘know’ are alien, and then destroy them.” Dr. Jesse Stoff,
The Prostate Miracle


Diagnosis of autoimmune diseases is based on symptoms and detection of antibodies (and/or very early T cells) reactive against antigens of tissues and cells involved. Antibodies against cell/tissue associated antigens are detected by immunofluorescence. Antibodies against soluble antigens are normally detected ELISA or radioimmunoassay (see table above). In some cases, a biological /biochemical assay may be used (e.g., Graves diseases, pernicious anemia).


The goals of treatment of autoimmune disorders are to reduce symptoms and control the autoimmune response while maintaining the body's ability to fight infections. Treatments vary widely and depend on the specific disease and symptoms: Anti-inflammatory (corticosteroid) and immunosuppressive drug therapy (such as cyclophosphamide, azathioprine, cyclosporine ) is the present method of treating autoimmune diseases.

Sources: Tolerance and autoimmunity;microbiology and immunology online.your immune system;immunedisorders.homestead.com;autoimmune disorder, lab test online.

Ps: Still couldn't get enough of this topic. haha

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