Autoimmune & Diagnostic ELISA (IVD)

About autoantibodies

While self-tolerance mechanisms normally protect an individual from potentially self-reactive lymphocytes, there are flaws. They result in an inappropriate response of the immune system against the auto components called autoimmunity.

Autoimmune diseases include more than 70 different disorders that affect approximately 5% of the population in Western countries. A large number of serum antibodies directed against functional cell structures (nucleic acid, nuclear molecules, receptors or other functional cellular components) can be detected in human autoimmune diseases; its presence plays a central role in the diagnosis and classification of these types of disorders.

Furthermore, several longitudinal cohort studies have shown that patients can carry autoantibodies many years before they manifest clinical symptoms, and the detection of these antibodies in serum has been shown to have great predictive value. Despite the growing knowledge of immunology during the last decades, more than one challenge regarding autoantibodies remains open, such as determining the mechanism involved in the breakdown of tolerance, as well as identifying the nature of autoimmune damage mediated by many of them.

Detection of autoantibodies under various conditions was the first element to support the role of the immune system in these autoimmune diseases. As antibodies were already well-known effector molecules, defining the pathogenic mechanisms of autoantibodies was one of the first aspects to be investigated. Mechanisms of autoantibody-mediated tissue/cell damage will be reviewed in Table 1.

Table 1 Mechanisms of action of autoantibodies

1. Induction of cell death (cytotoxicity) after cell binding of autoantibodies

  • Complement-mediated cell death
  • Antibody-dependent cell-mediated death
  • Phagocytosis by the mononuclear phagocyte system

2. Binding to cell surface receptors without cytolysis

  • Modulation of cell surface receptors.
  • Blockade of cell surface receptors.
  • Stimulation of cell surface receptors.

3. Immune complex-mediated damage

4. Translocation of intracellular antigens to the cell membrane.

  • Cross-reactions between intracellular and membrane antigens.
  • Intracellular antigen translocation after cell injury or activation.

5. Penetration into living cells

6. Binding to extracellular molecules

  • Binding to surface membranes and subsequent destruction of cells is a well-established pathogenetic mechanism of autoantibodies. This cell death (cytolytic or apoptotic) can involve mechanisms mediated by complement, mediated by ADCC (mainly through NK or CD8 + lymphocytes) or mediated by phagocytes (opsonization).
  • Binding to cell surface molecules and subsequent modification of their cellular biological activity (especially when the molecule is a receptor) without cell death is another well-established direct pathogenetic mechanism of some autoantibodies. This modification of cell activity can occur by modulation, blocking or stimulation of cell surface receptors and is usually the main pathogenic process that explains most autoimmune diseases.
  • IC formation and tissue localization can occur under autoimmune conditions by two different mechanisms: (1) local IC formation, as occurs in farmer’s lung (sometimes by direct reaction with structural antigens in local tissue); and (2) deposition of circulating ICs, as in certain glomerulonephritis (ie, lupus nephritis).
  • Some autoantibodies against intracellular proteins can bind to cell surface membranes. The two main proposed mechanisms are cross-reactions between intracellular and membrane antigens and translocation of intracellular antigen to the membrane after cell injury or activation.
  • There is some evidence that a few autoantibodies can penetrate living cells and others can bind to extracellular molecules.


  • Anti-neutrophil antibodies

1. Myeloperoxidase autoantibody
2. Proteinase 3 autoantibody

  • Antinuclear antibodies

1. Anti-U1RNP and anti-Sm antibodies
2. Anti-dsDNA autoantibodies
3. Anti-Ro / SSA autoantibodies
4. Anti-SS-B (La) autoantibodies
5. Autoantibodies to topoisomerase I (SCL 70)

  • Autoantibodies against rheumatic diseases

1. Autoantibodies against C1q
2. Rheumatoid factors
3. Antibodies against citrus proteins

  • Endocrine autoantibodies

1. Thyroid autoantibodies: antibodies against thyroid peroxidase and thyroglobulin
2. Thyrotropin receptor antibodies
3. Glutamic acid decarboxylase antibody
4. Other autoantibodies in type 1 diabetes mellitus

  • Neurological system autoantibodies

1. Muscle-specific acetylcholine receptor and kinase autoantibodies
2. Myelin oligodendrocyte glycoprotein (MOG) autoantibody

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