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Vaccination and autoimmune disease: what is the evidence?

For personal use. Only reproduce with permission from The lancet Publishing diseases affect about 5% of individuals indeveloped the prevalence of mostautoimmune diseases is quite low, their individualincidence has greatly increased over the past few years, asdocumented for type 1 diabetes2,3and multiple autoimmune disorders arise in individuals in age-groups that are often selected as targets for vaccinationprogrammes. Therefore, in the context of an increasingnumber of Vaccination episodes, coincidence of eventsshould be expected.

Jun 03, 2003 · For personal use. Only reproduce with permission from The Lancet Publishing Group. In theory, one could propose that any microbe expressing an epitope that could serve as …

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Transcription of Vaccination and autoimmune disease: what is the evidence?

1 For personal use. Only reproduce with permission from The lancet Publishing diseases affect about 5% of individuals indeveloped the prevalence of mostautoimmune diseases is quite low, their individualincidence has greatly increased over the past few years, asdocumented for type 1 diabetes2,3and multiple autoimmune disorders arise in individuals in age-groups that are often selected as targets for vaccinationprogrammes. Therefore, in the context of an increasingnumber of Vaccination episodes, coincidence of eventsshould be expected.

2 The potential interactions betweenvaccines and autoimmune diseases have become a commontopic of claims and counter claims, and questions are oftenraised with respect to the potential risk of autoimmunediseases after Vaccination . Some of these questions havebeen selected by the WHO Vaccine Safety AdvisoryCommittee for further research (panels 1, 2, and 3).5 Ouraim is to provide a rational approach to answer thesefrequent queries. Autoimmunity is generally assumed to result fromcomplex interactions between genetic traits andenvironmental often, autoimmuneresponses are not followed by any clinical manifestationsunless additional events favour disease expression eg, alocalised inflammatory process at tissue level.

3 Anunderstanding of the mechanisms by which autoimmuneresponses are generated and of how they might or mightnot lead to autoimmune diseases is of paramountimportance in defining the real risk of vaccine-associatedautoimmunity. Infections are usually considered as keyelements in the control of immune responses, and there isevidence that they might either precipitate or preventautoimmune we analyse ourunderstanding of how infections can lead to autoimmunedisease and thus assess the relative risk of autoimmunedisease arising as a consequence of online June 3, 2003 of Pathology and Microbiology, University of Bristol,Bristol, UK(Prof D C Wraith PhD).

4 Department of Immunology,H pital Erasme, Brussels, Belgium(Prof M Goldman MD); andCentre of Vaccinology, Department of Pathology, University ofGeneva, Switzerland (Prof P-H Lambert MD)Correspondence to:Prof David C Wraith, Department of Pathologyand Microbiology, University of Bristol, Bristol BS8 1TD, UK (e-mail: autoimmune disease and infection Human beings have a highly complex immune systemthat evolved from the fairly simple system found ininvertebrates. The so-called innate invertebrate immunesystem responds non-specifically to infection, does notinvolve lymphocytes, and hence does not displaymemory.)

5 The adaptive immune system, shared byvertebrates, displays both specificity and memory, and isdesigned to provide protection against almost allinfections. Furthermore, polymorphisms in genes thatcontrol the immune system ensure that the species as awhole can generate sufficient immunological diversity tosurvive any new infectious drawback to such a broadly responsive defencemechanism is the possibility that, in responding toinfection, the immune system of a few individuals willturn against their own tissues, thus causingautoimmunity.

6 One could argue that the immune systemshould have evolved mechanisms that would allow it torespond only to infectious agents and not there are mechanisms by which many self-reactive lymphocytes are removed from the immunerepertoire of the adaptive immune system. Thus, self-reactive B cells are deleted in the bone marrow, and self-reactive T cells are deleted in the thymus , it is noteworthy that an immunesystem from which all self-reactive lymphocytes aredeleted would not provide a sufficiently broad repertoireto combat infection can induce or trigger autoimmunedisease via two mechanisms antigen-specific or antigennon-specific which can operate either independently ortogether.

7 An autoimmune disease will only arise,however, if the individual is genetically predisposed tothat particular condition. Vaccination and autoimmune disease: what is the evidence? David C Wraith, Michel Goldman, Paul-Henri LambertReviewTHE lancet Published online June 3, 2003 many as one in 20 people in Europe and North America have some form of autoimmune disease. These diseasesarise in genetically predisposed individuals but require an environmental trigger. Of the many potential environmentalfactors, infections are the most likely cause.

8 Microbial antigens can induce cross-reactive immune responses againstself-antigens, whereas infections can non-specifically enhance their presentation to the immune system. The immunesystem uses fail-safe mechanisms to suppress infection-associated tissue damage and thus limits autoimmuneresponses. The association between infection and autoimmune disease has, however, stimulated a debate as towhether such diseases might also be triggered by vaccines. Indeed there are numerous claims and counter claimsrelating to such a risk.

9 Here we review the mechanisms involved in the induction of autoimmunity and assess theimplications for Vaccination in human beings. Search strategyWe did a computer-aided search of PubMed and ISI Web ofScience, using the search terms: vaccine and autoimmunedisease, and Vaccination and autoimmune disease. Thissearch provided a list of published work up to August, 2002,which we used to supplement our existing knowledge of theprimary published work on the subject. We did not limit oursearch to articles published in personal use.

10 Only reproduce with permission from The lancet Publishing mimicryA popular explanation for how infectious agentsstimulate autoimmunity in an antigen-specific way is viamolecular determinants of micro-organisms can thus be recognised by the host immunesystem as being similar to antigenic determinants of the host itself (figure 1). Molecular mimicry amongsugar structures is common and leads to numerousmanifestations of infection-associated and antibody-mediated ,11 For example, about a third ofall cases of Guillain-Barr syndrome are preceded byCampylobacter jejuni bacterium expressesa lipopolysaccharide molecule that mimics variousgangliosides present in high concentrations in peripheralnerves.


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