Molecular mimicry between microbial antigens and host tissue forms an attractive hypothetical mechanism for the triggering of autoimmune disease by preceding infections. A proposed mechanism that could have been misinterpreted for molecular mimicry is the expression of dual t cell receptors tcr on a single t cell. Summary virus infections and autoimmune disease have long been linked. Molecular mimicry a popular explanation for how infectious agents stimulate autoimmunity in an antigenspecific way is via molecular mimicry. Pdf molecular mimicry as a mechanism of autoimmune disease. Usually a single organ or individual cell type is avected in the absence of gross abnormalities of the immune system. The induction of an immune response to the microbial antigens results in a crossreaction.
Molecular mimicry has been found to be critical in pathogenesis of arf as. Module autoimmunity and autoimmune diseases microbiology 576 notes glands or it may involve particular cellstissues all over the body when it is. Molecular mimicry as a mechanism of autoimmune disease matthew f. Environmental factors and a genetic predisposition result in tissue injury caused by autoreactive t cells or antibodies. Molecular mimicry has offered a merit to initiate an autoimmune reaction and has been touted as the putative mechanism for both lyme neuroborreliosis, a neurological manifestation of the pathogen and lyme arthritis, which occurs as a delayed sequel to infection.
Molecular mimicry that primes for autoimmunity which is. Steffrell a, schubart a, storch m, amini a, mather i, lassmann h, linington c. Molecular mimicry in autoimmune disease susan leech the origins of autoimmune disease are multifactorial. The loss of immune regulation during responses against microbial antigens may explain development of. Thus, molecular mimicry initiated as a host response to a virus or a microbial infection, but alternatively crossreacting with an appropriate hostantigen, can be a mechanism for instigating an autoimmune disease. Autoimmunity the term autoimmunity is often erroneously used for any disease in which immune reactions accompany tissue injury, even though it may be difficult or impossible to establish a role for immune responses against self antigens in. An autoimmune disease is a case of mistaken identity. Autoimmunity in rheumatic diseases is induced by microbial. Molecular mimicry how eating animal based products causes autoimmune disease autoimmune disease rates increasing. The growing prevalence of autoimmune diseases ought to cause us to wonder what the mechanism is behind the growth and prevalence.
Molecular mimicry and t cellmediated autoimmune disease. Molecular mimicry an overview sciencedirect topics. Mechanisms of autoimmunity cellular and molecular immunology a. Review article from the new england journal of medicine molecular mimicry and autoimmunity. These t cells have dual reactivity to both foreign and selfantigens leaving the host vulnerable to foreign insults capable of triggering an autoimmune response. Results structural characterization of the immunodominant. It is thought that damage could result from an immune response to similar regions shared between virus and the.
Molecular mimicry of this immunodominant selfpeptide by viruses therefore pre sents a possible mechanism for the induction of autoimmu nity in ms. Abstract molecular mimicry has been proposed as a pathogenetic mechanism for autoimmune disease, as well as a probe useful in uncovering its etiologic agents. It is possible therefore, that t cells primed by a foreign antigen may be able to recognise a related, but not identical, peptide from a selfantigen. Although several means have been hypothesized to play a role in disease, a widely accepted mechanism for viralinduced autoimmunity is molecular mimicry. Butyrophilin, a milk protein, modulates the encephalitogenic t cell responses to. Three way molecular mimicry has been shown to exist between. Autoimmune disease is the consequence of an immune response against selfantigens that results in. Molecular mimicry definition of molecular mimicry by. N2 a variety of mechanisms have been suggested as the means by which infections can initiate andor exacerbate autoimmune diseases. Molecular mimicry is characterized by an immune response to an. Molecular mimicry is one of the leading mechanisms by which infectious or chemical agents may induce autoimmunity. The hypothesis is based in part on the abundant epidemiological, clinical,andexperimental evidence of an association of infectious agents with autoimmune disease and observed cross.
Autoimmunity due to molecular mimicry as a cause of. The hypothesis is based in part on the abundant epidemiological, clinical, and experimental evidence of an association of infectious agents with autoimmune disease and observed crossreactivity of immune reagents with host self antigens and. Mechanism of autoimmune diseases flashcards quizlet. These infections often precede the occurrence of inflammation in the target organ. The selfrecognition mechanisms are no exception, and a number of disease have been identified in which there is autoimmunity, due to copious production of autoantibodies and. Molecular mimicry is a mechanism by which immunological self tolerance can be broken, leading to autoimmune disease. B cell epitope spreading after molecular mimicry is a mechanism by which the body likely begins to break selftolerance, leading to the development of autoimmune disease. With respect to the mechanisms by which the molecular mimicry at. In such cases infection may trigger autoimmune disease.
Molecular mimicry in autoimmune disease archives of disease in. T1 molecular mimicry as a mechanism of autoimmune disease. Inflammation induced by exposure to a foreign antigen can lead to autoimmune diseases from crossreactive epitopes molecular mimicry. Molecular mimicry and autoimmunity arthritis research. Autoantibodies to hla b27 in the sera of hla b27 patients. Pdf molecular mimicry is one of the leading mechanisms by which infectious.
Epitope mimicry may indeed be involved in the pathogenesis of. Molecular mimicry in autoimmune disease archives of. One hypothesis that couples infection with autoimmune disease is molecular mimicry. Microbial infection may initiate autoimmune response not only through molecular mimicry, but also with polyclonal activation and release. In this article we summarize some of the areas of current research that may eventually clarify the mech anisms by which infectious agents could act as the inciting agents of autoimmune diseases. In conclusion, the findings reported by hemmer et al. Molecular mimicry provides an explanation for the genetic observation that identical twins rarely manifest the same autoimmune. Many mechanisms may account for immunemediated pathology after viral infections. An explanation for autoimmune diseases and infertility. Several mechanisms often used to explain the association of autoimmunity and virus infection are molecular mimicry, bystander activation with or without epitope spreading, and viral persistance. Autoimmune disease is the consequence of an immune response against selfantigens that results in the damage and eventual dysfunction of target organs.
Unfortunately, there are a variety of mechanisms including molecular mimicry, bystander activation, exposure of cryptic antigens, and superantigens by which pathogens can aid in the expression of an autoimmune disease 1621. Molecular mimicry as a mechanism of autoimmune disease. We have established a model where viruses can prime animals for autoimmune cns disease by a mechanism of molecular mimicry. A variety of mechanisms have been suggested as the means by which infections can initiate andor exacerbate autoimmune diseases. With an increased amount of research, there has been tremendous growth in the study of the several different ways in which autoimmunity can occur, one of. Evidence suggests that microorganisms contain proteins which are similar enough to host proteins that they can stimulate existing b and t cells to respond to self proteins. Molecular mimicry between pathogen and host has been proposed as a mechanism for the development of autoimmune diseases.
Pdf molecular mimicry and autoimmunity researchgate. Our current knowledge of the detailed mechanisms of molecular mimicry is limited by the issues of prolonged periods of latency before the appearance of disease. Molecular mimicry is the main pathogenetic mechanism that can explain these forms of microbedisease associations, where the causative microbes can initiate the disease with consequent productions of antibacterial and crossreactive autoantibodies which have a great impact in the propagation and the development of these diseases. Over 30 years ago, molecular mimicry by either a virus or bacteria was hypothesized to initiate and exacerbate an autoimmune response through sequence or structural similarities with selfantigens. Any disease that results from such an aberrant immune response is termed an autoimmune disease. Molecular mimicry has been proposed as a pathogenetic mechanism for autoimmune disease, as well as a probe useful in uncovering its etiologic agents. Autoantibodies to hla b27 in the sera of hla b27 patients with ankylosing spondylitis and reiters syndrome. Mimicry of host antigens by infectious agents may induce crossreactive autoimmune responses to epitopes within host proteins which, in susceptible individuals, may tip the balance of immunological response versus tolerance toward response and subsequently lead to autoimmune disease. Currently, molecular mimicry is the prevailing hypothesis as to how viral antigens initiate and maintain autoimmune responses which lead to specific tissue. It occurs when similarities between foreign and selfpeptides favor an activation of autoreactive t or b cells by a foreignderived antigen in a susceptible individual. Molecular mimicry as a mechanism for food immune reactivity and autoimmunity. Autoimmunity is the system of immune responses of an organism against its own healthy cells and tissues.
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