Proving a disease is autoimmune: transfer of autoantibodies
Transferring patient autoantibodies (antibodies against the body's own tissues) into a healthy host (the recipient) and reproducing the disease is the strongest evidence that it is autoimmune.
Remember
If patient autoantibodies given to a healthy host reproduce the disease, they have shown that they can cause it, which makes this the strongest evidence of an autoimmune cause. Presence of autoantibodies, their location at the damaged site and response to immunomodulatory therapy (drugs that adjust immune activity) are supportive but weaker.
Finding an autoantibody (an antibody that reacts against the body's own tissues) in a patient does not prove that it causes the disease. Autoantibodies can be present without causing disease, for example when they are a result of the damage. So a disease is classified as autoimmune more strictly than by simply finding an autoantibody.
The usual criteria are that autoantibodies or autoreactive T cells (T cells that react against self) are present, that they are found at the site of tissue damage, and that there is clinical improvement on immunomodulatory therapy (drugs that adjust immune activity). Each of these is supportive rather than proof of cause.
The strongest proof is passive transfer. Antibodies (or autoreactive T cells) from affected patients are given to a healthy recipient, and if the same disease appears, they are pathogenic, meaning they actually cause disease and do not merely accompany it. This is called direct evidence. Immunising an experimental animal with a self antigen (an antigen from the body's own tissues) so that it develops the disease counts as indirect evidence, and circumstantial evidence comes from clinical clues.
Experimental models can show transfer, and routine clinical diagnosis does not require it. Even so, when it is available, it is the most convincing finding.
Key facts
- Strongest evidence
- Patient autoantibodies given to a healthy host reproduce the same disease.
- What it proves
- The antibodies can cause the disease and do not just accompany it.
- Ranking
- Direct evidence (transfer to a healthy host) ranks above indirect evidence (disease reproduced in an animal by immunising it with the self antigen) and circumstantial evidence (clinical clues).
- Weaker findings
- Presence of autoantibodies or autoreactive T cells, their location at the damaged site and response to immunomodulatory therapy are supportive rather than proof of cause.
- Where it is used
- In experimental models and research, not as a requirement for routine clinical diagnosis.
Exam traps
- Autoantibodies in patients are circumstantial rather than direct proof, since some autoantibodies are also found in healthy people and autoantibodies can be present without causing disease.
- Reproducing a disease in an experimental animal by immunisation with a self antigen is indirect evidence, which supports autoimmunity, though it is not as strong as transferring pathogenic antibodies or T cells to a healthy host.
- Improvement on non-steroidal anti-inflammatory drugs does not point to autoimmunity, because such drugs reduce inflammation of any cause.
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