Our immune system is a robust defensive network, fighting against pathogens that enter our body and protecting us from severe infection. But sometimes, all does not go according to plan, and the focus of attack is our own body’s cells and tissues.
These instances of aberrant immune responses, known as autoimmune conditions, are quite prevalent globally. In some instances, the bacteria and viruses we are exposed to are the culprits.
The link between pathogens and autoimmune disorders can be described by a number of mechanisms.
Molecular mimicry: sometimes, a given bacteria or virus is composed of molecules or components that are similar to those found in the host, meaning B and T cells are activated that have the capacity to recognize and attack parts of the host.
Bystander activation: infection is inherently inflammatory in nature, and the cytokines generated during such events have the potential to activate and drive the proliferation of auto-reactive T cells that are specific to components from the host itself.
Epitope spreading: sometimes, by chance, host components are in close proximity to microbes and their respective components, and the immune response to the microbes expands to the secondary epitopes found in the host.
Rather remarkably, some extremely common autoimmune conditions have inextricable links to pathogens.
Multiple sclerosis: Myelin basic protein and myelin glycoprotein oligodendrocytes are quite similar to some of the proteins expressed by Epstein Barr virus, meaning that infection with the gammaherpesvirus sometimes leads to the generation of antibodies that target one of the core building blocks of our central nervous system.
Type 1 Diabetes: Sequence homology has been demonstrated between glutamic acid decarboxylase (GAD) and various proteins found in viruses like CMV and EBV. Interestingly, GAD has been found to be targeted by self-reactive antibodies in cases of T1D.
What is most empowering, however, is that there is hope. If viruses and bacteria (and other pathogens) are drivers of chronic conditions beyond infection, the prevention of infection may well allow for the prevention of onset of debilitating conditions like MS and prevalent ones like T1D.
It is crucial that the paradigm of vaccination is understood not only from the standpoint of infectious disease and pandemics, but the broader conditions, morbidity, and mortality that infectious agents contribute to; perhaps, one day, we’ll not only be vaccinating ourself against the flu, but also against diabetes and MS – thereby lowering the likelihood of developing these conditions by eliminating probable contributors.
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