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Microbes & Immunity Infectious agents and autoimmune diseases

sclerosis) that already carry the pathogen’s “imprint.” Moreover, the role of molecular mimicry, which is
Meanwhile, viruses or bacteria, which have not been considered “one of the leading mechanisms by which
eliminated, alter previously unaffected cells, which then infectious or chemical agents may induce autoimmunity,”
become targets of the immune system. as stated by Rojas et al., 12(p100) can be seen from a different
point of view, in the framework of the proposed conceptual
Relapsing-remitting forms of autoimmune diseases
in the proposed conceptual model can be understood model. The basic idea is that autoimmune cells mistake
as follows: the end of a relapsing phase occurs when the self-cells as foreign, due to similarities between the host’s
number of cells bearing a detectable pathogen’s “imprint” protein structures and those of invading bacteria or
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falls below a threshold, which varies depending on viruses. For instance, Bacteroides fragilis, a member of the
the specific disease. The cessation of the inflammatory normal human gut microbiota, encodes a protein similar
phase provides relief for the patients. Moreover, it may to human ubiquitin and could trigger an autoimmune
response. There is an increase in evidence on the ability
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be accompanied by a certain degree of recovery, which
depends on the resilience of the affected tissues, organs, or of bacteria to mimic human proteins and contribute
systems, particularly their regenerative capacity. to the onset of autoimmune diseases and their related
clinical implications. However, molecular mimicry may
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Nevertheless, the infectious agents have not been also have the “opposite” effect, allowing pathogens to
completely eliminated, and the “imprinting” process evade the host’s immune response. 39,40 This effect could
persists. During the remitting phase, this process remains be regarded as more predictable. The model, discussed
undetected, while its rate might be lower than repair/ in this paper, might offer the “missing link” between the
regeneration. Symptoms reemerge when cumulative two possible effects of molecular mimicry. During the first
cellular damage, due to the attack of the immune system on stage, the “invaders” avoid attacks by the immune system
altered cells, exceeds a certain threshold. New infections and can cause alterations to the host’s cells. Subsequently,
by pathogens may facilitate the onset of the subsequent when the immune system can recognize them, it targets
relapsing phase by accelerating the “imprinting” process the “invaders” along with the cells with the pathogens’
and/or by reactivating the patients’ immune system. “imprint.” This two-stage process can explain the time lag
Autoimmune diseases with good prognosis are between infection and autoimmune response, as it takes
considered cured when the immune system (naturally or some time for the infectious agents to affect a substantial
with the support of antiviral drugs or antibiotics, as in number of cells to a degree detectable by the immune
Sydenham chorea) successfully eliminates the infectious system. In the same framework, time-lag differences from
agents, halting further cellular alteration. The degree of disease to disease (and even from case to case for the same
residual damage depends on the resilience of the affected disease) can also be explained, as different infectious agents
system. may be involved.
Notably, the role of resilience in general can be Another important issue, related to many autoimmune
distinguished according to three types: diseases, is epitope spreading. 41,42 As summarized by
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(i) Degree of damage from a given stress. In resilient Cornaby et al., epitope spreading can be triggered by
systems, the damage does not completely inhibit the assorted viruses, bacterial infections, and stress. The
functioning of the stressed system. occurrence can be justified in the conceptual model
(ii) Speed of recovery from damage that has occurred framework presented in this paper. As the alteration of
(iii) The ability to substitute damaged parts with others infected cells evolves over time, it is reasonable to expect
that undertake the function of the damaged ones. This that the autoimmune response may target different
is particularly important in network structures, either epitopes within the same antigen, a phenomenon known
biological or artificial. In most cases, a system that has as epitope spreading.
recovered functionally is less resilient than before the Finally, the role of the persistence of infectious agents
damage. is adequately explained, as their continued existence is
Regarding the autoimmunity challenges discussed essential for the continuation of the “imprinting” process.
in this paper, the first and third types of resilience may 4. The proposed model and other factors
contribute to the time lag between infection and detection
of autoimmune response. Moreover, the second and related to autoimmune responses
third types contribute to patients’ temporal recovery The roles of genetic predisposition, sex, dietary habits,
or permanent cure, in remitting-relapsing and good- stress, and lifestyle in developing autoimmune responses
prognosis autoimmune diseases, respectively. are well documented. These roles, together with the

Volume 2 Issue 4 (2025) 20 doi: 10.36922/MI025100017