Is There Such a Thing as Autoimmunity?

Autoimmunity occurs whenever the immune system attacks host tissue. The number of autoimmune diseases is believed to have reached the staggering figure of 80 and, mind, this is only according to the most conservative counting. The reason for the wide spread of autoimmune conditions is that any part of the body can become a potential target for destruction: from organs like kidneys and hearts, to glands like the thyroid and the pancreas, and even individual cells, as in the case of the red blood cells.

Now, the dominant framework for understanding the pathology of autoimmunity used to rely very much on the idea that, due to a certain environmental trigger and genetic predisposition, the immune system gets a bit confused and wrongly attacks certain parts of its host's body. Thus, autoimmunity was conceived as a malfunctioning of the immune system and most therapies have been designed as a way to fight against the activation of the immune response and to neutralize its effects on the body. Like inflammation, for instance. According to this perspective, the immune system, in its ignorance, is the villain.

But what if this was not the case? What if the immune system didn't wrongly attack the host tissue? What if it had a reason to do it? So many 'what ifs', but actually recent research does emphasize more and more the correlation between viral and bacterial triggers and what we call autoimmunity. In this sense, what falls under the label of autoimmunity is essentially a normal immune response, in which the body is expected to build a defense against external pathogens.

Fujinami et al. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360274/) present three mechanisms through which infections may initiate immunoreactivity: 

1. Molecular mimicry: shared immunologic epitope (the part of an antigen which is recognized by the immune system) between the microbe and the host.
2. Bystander activation: activation of antigen-presenting cells, which leads to a T-cell response.
3. Viral persistence: constant presence of the viral antigen driving the immune response.

The most compelling evidence, however, for rethinking the concept of autoimmunity and for accommodating better the role that infections play in relation to it is to look at the long and non-exhaustive list of autoimmune conditions that are correlated with bacterial and viral triggers. 

• Cardiomyopahty: coxsackievirus B; Streptococcus pyogenes; Trypanosoma cruzi, Borrelia burgdorferi
• Herpetic stromal keratitis: herpes simplex virus
• Uveitis: Escherichia coli
• Type 1 diabetes: rubella
• Guillain-Barre syndrome: Campylobacter jejuni; Mycoplasma pneumoniae,; Haemophilus influenzae
• Multiple sclerosis: Chlamydia pneumoniae; herpes simplex virus; human papillomavirus; adenovirus
• Alopecia areata: H1N1 virus; Epstein-Barr virus; hepatitis B vaccine; Helicobacter pylori 
• Atopic dermatitis: Staphylococcus aureus 
• Celiac disease: rotavirus
• Hashimoto's thyroiditis: hepatitis C virus; human parvovirus B19; coxsackievirus B; herpes simplex virus
• Narcolepsy: H1N1 virus
• Psoriasis: human immunodeficiency virus; streptococcal infections in the upper respiratory tract; an uncommon strain of human papillomaviruses, called EP-HPVl; Helicobacter pylori 
• Rheumatoid arthritis: Epstein-Barr virus; human herpes virus 6
• Systemic lupus erythematosus: Epstein-Barr virus

I have presented only some of the most spread or well-known autoimmune conditions. The complete list, however, is much larger than this.  What it shows, nonetheless, is a certain direction in the study of autoimmunity. Thus, any successful advancement in the treatment of autoimmunity would have to rely on the following considerations:

1. Focus on really treating autoimmune conditions and not only on the alleviation of their symptoms. This can only be achieved if we understand their root cause, which brings me to points 2 and 3.

2. Map out the exact environmental triggers for each autoimmune condition.

3. Find out which genetic markers are associated to autoimmunity.

4. Deliver personalized medical advice to the people that present a certain genetic marker, especially relevant when it comes to the types of vaccinations that these people could receive or not. It is especially tricky nowadays to manifest any concerns related to the effects of vaccinations or refuse to be vaccinated, when there are so many organizations and individuals militating against vaccinations on pseudo-scientific or even completely non-scientific grounds. In spite of this and looking at the available evidence, people suffering form autoimmune conditions or having the genetic predisposition for autoimmunity should have personalized vaccination schemes. Which means that, in some cases, they would have to forego vaccines.

Further reading:

L. G. Delogu et al., 'Infectious diseases and autoimmunity' (2011)
http://www.ncbi.nlm.nih.gov/pubmed/21997935

A. M. Ercolini and S. D. Miller , 'The role of infections in autoimmune disease' (2009)  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665673/

R.S Fujinami et al., 'Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease' (2006)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360274/

V. Molina and Y. Schoenfeld, 'Infection, vaccines and other environmental triggers of autoimmunity' (2005)
http://www.ncbi.nlm.nih.gov/pubmed/16126512