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Microbes & Immunity Infectious agents and autoimmune diseases

4.5. Stress essential role in regulating immune responses. Therefore,
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It has been known for many years that stress (mainly the appearance of such IRAEs could be expected, at least
chronic stress) can cause immunosuppression. It may in the form of exacerbation of pre-existing autoimmune
59
also increase the risk or exacerbation of autoimmune diseases. However, seemingly unrelated cells (tissues or
organs) are also affected in certain instances. A possible
diseases, 7,59-62 which entail increased immune system explanation, closely related to the proposed model of
activity. This apparent contradiction can be resolved in autoimmune diseases, is that a similar, but distinct, process
the framework of the proposed mechanism: in the first
stage, stress-induced weakness of the immune system takes place in the second case. The underlying similarity is
facilitates cell “imprinting” by pathogens. During the later that the affected cells are not completely healthy. In the first
stage, the immune system recognizes mounting alterations case, the attacked cells bear the “imprint” of the pathogen,
linked to a prior infection. In contrast, in the second case,
of the affected cells and attacks them. This two-stage they bear a slight cancerous alteration, which cannot be
process allows for a time lag between stress periods and detected with current diagnostic means. The “boosted”
exacerbations of autoimmune diseases.
immune system, on detecting alterations, even slight ones,
4.6. Treatment of multiple sclerosis with IFNβ attacks the affected cells, irrespective of the alteration’s
cause.
IFNβ is mildly effective in treating the relapsing-
remitting form of multiple sclerosis. However, the precise 6. Conclusion
mechanisms through which IFNβ achieves its therapeutic
effects are not fully understood. 63,64 The proposed conceptual model, which attributes
autoimmune diseases to progressive alteration of host
IFNs are known to stimulate cells infected by viruses cells caused by infectious agents, can explain many aspects
to produce proteins that prevent virus replication within of these diseases. If this model proves valid, halting the
them, eventually hindering infections. The complex IFN progression or even curing autoimmune diseases may
contribution to combating cancer-associated viruses be possible by developing new antibiotics or antiviral
remains an active area of ongoing research. 65 drugs. These drugs should aim to completely eliminate
Given the undisputed antiviral properties of IFNs, the infectious agents that cause cell alterations, rendering
irrespective of the exact mechanism, the therapeutic effect them immune system targets.
of IFNβ on multiple sclerosis can be reasonably related to Halting the progress of an autoimmune disease does
its infection-stemming properties. This fits perfectly in the not result in the spontaneous restoration of damaged
framework of the proposed model, which attributes the tissues. As mentioned in Section 3, the degree of residual
evolution of autoimmune diseases to residual infectious damage depends on the resilience of each affected system.
agents. As the disease has been related to different infectious For this reason, it seems reasonable to combine antibiotics
agents, variations in the efficiency of their treatment with or antiviral therapies with immunomodulatory agents to
IFNβ could be attributed, at least partially, to the virus reduce progressive damage until the underlying infectious
involved in each case. cause is eliminated. Once the infectious agents are fully
eradicated, continued use of immunomodulatory drugs
5. Drug-induced autoimmunity may become unnecessary, or, at the very least, redundant.
Some drugs have been linked to triggers of autoimmune
diseases, such as SLE and rheumatoid arthritis. The 7. Directions for further research
5,66
exact mechanism of drug-induced autoimmunity is still The following research directions would be very helpful
unknown. A case, which could reasonably be explained to validate (or partially validate) the proposed conceptual
in the framework of the proposed conceptual model, is model of the mechanism underlying autoimmune diseases,
discussed in the following paragraph. and to establish new treatment protocols, to the extent that
the model proves accurate:
5.1. Treatment of malignancy (i) Further statistical studies on the temporal correlation
Some new treatments for malignancy have been related to between the first manifestation or seizures of
autoimmunity. These treatments use immune checkpoint autoimmune diseases and infections from viruses or
inhibitors (CPIs) to facilitate the patient’s immune system bacteria.
to attack cancer cells. Side effects include a range of (ii) Clinical trials of existing and new antibiotics or
immune-related adverse events (IRAEs), from neurological antiviral drugs to stop the further progression of
effects 67,68 to rheumatological effects. CPIs play an autoimmune diseases and eventually cure them.
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Volume 2 Issue 4 (2025) 22 doi: 10.36922/MI025100017