Novel proteins entering the food chain, for example by genetic modification of plants, have to be tested for allergenicity. Allermatch™ http://allermatch.org
 is a webtool for the efficient and standardized prediction of potential allergenicity of proteins and peptides according to the current recommendations of the FAO/WHO Expert Consultation, as outlined in the Codex alimentarius. A query amino acid sequence is compared with all known allergenic proteins retrieved from the protein databases using a sliding window approach. This identifies stretches of 80 amino acids with more than 35% similarity or small identical stretches of at least six amino acids. The outcome of the analysis is presented in a concise format. The predictive performance of the FAO/WHO criteria is evaluated by screening sets of allergens and non-allergens against the Allermatch databases. Besides correct predictions, both methods are shown to generate false positive and false negative hits and the outcomes should therefore be combined with other methods of allergenicity assessment, as advised by the FAO/WHO. Allermatch™ provides an accessible, efficient, and useful webtool for analysis of potential allergenicity of proteins introduced in genetically modified food prior to market release that complies with current FAO/WHO guidelines.

https://link.springer.com/content/pdf/10.1186%2F1471-2105-5-133.pdf

Allermatch™, a webtool for the prediction of potential allergenicity according to current FAO/WHO Codex alimentarius guidelines

The role of autoimmunity in atopic dermatitis (AD) is unclear. We sought to critically examine the occurrence, correlation with severity, and possible causative role of autoreactivity in patients with AD. Our systematic review of studies identified from MEDLINE included 31 experiments that described autoreactivity in patients with AD. We defined autoreactivity as in vitro or in vivo evidence of immune response to autologous human, generic human, or recombinant human proteins or other tissue/cellular components. Autoreactivity prevalence in patients with AD ranged from 23% to 91% in 14 studies involving 2644 participants, although it did not appear to vary with age, sex, or disease duration. In contrast to studies of AD, IgE autoreactivity was not found in healthy subjects or in those with allergic rhinoconjunctivitis, psoriasis, systemic lupus erythematosus, or other inflammatory diseases (8 studies of 816 participants). Two reports found a positive correlation between autoreactivity and AD severity. We suggest that autoreactivity might be playing a causative role in AD based on the magnitude and specificity of the associations found; plausible mechanisms through IgE autoantibodies, IgG autoantibodies, and T H 1 autoreactivity; and experimental elicitation of eczematous lesions after provocation. Whether autoantibodies contribute to AD chronicity now needs to be examined in longitudinal studies.

https://www.jacionline.org/article/S0091-6749(12)00263-1/pdf

Does “autoreactivity” play a role in atopic dermatitis?

The study of autoimmunity mediated by immunoglobulin E (IgE) autoantibodies, which may be termed autoallergy, is in its infancy. It is now recognized that systemic lupus erythematosus, bullous pemphigoid (BP), and chronic urticaria, both spontaneous and inducible, are most likely to be mediated, at least in part, by IgE autoantibodies. The situation in other conditions, such as autoimmune uveitis, rheumatoid arthritis, hyperthyroid Graves' disease, autoimmune pancreatitis, and even asthma, is far less clear but evidence for autoallergy is accumulating. To be certain of an autoallergic mechanism, it is necessary to identify both IgE autoantibodies and their targets as has been done with the transmembrane protein BP180 and the intracellular protein BP230 in BP and IL-24 in chronic spontaneous urticaria. Also, IgE-targeted therapies, such as anti-IgE, must have been shown to be of benefit to patients as has been done with both of these conditions. This comprehensive review of the literature on IgE-mediated autoallergy focuses on three related questions. What do we know about the prevalence of IgE autoantibodies and their targets in different diseases? What do we know about the relevance of IgE autoantibodies in different diseases? What do we know about the cellular and molecular effects of IgE autoantibodies? In addition to providing answers to these questions, based on a broad review of the literature, we outline the current gaps of knowledge in our understanding of IgE autoantibodies and describe approaches to address them.

/pdf/immunoglobulin-e-mediated-autoimmunity-5auj21m6yb.pdf

Immunoglobulin E-Mediated Autoimmunity.

The pathophysiology of atopic dermatitis (AD) is highly complex and understanding of disease endotypes may improve disease management. Immunoglobulins E (IgE) against human skin epitopes (IgE autoantibodies) are thought to play a role in disease progression and prolongation. These antibodies have been described in patients with severe and chronic AD, suggesting a progression from allergic inflammation to severe autoimmune processes against the skin. This review provides a summary of the current knowledge and gaps on IgE autoreactivity and self-reactive T cells in children and adults with AD based on a systematic search. Currently, the clinical relevance and the pathomechanism of IgE autoantibodies in AD needs to be further investigated. Additionally, it is unknown whether the presence of IgE autoantibodies in patients with AD is an epiphenomenon or a disease endotype. However, increased knowledge on the clinical relevance and the pathophysiologic role of IgE autoantibodies and self-reactive T cells in AD can have consequences for diagnosis and treatment. Responses to the current available treatments can be used for better understanding of the pathways and may shed new lights on the treatment options for patients with AD and autoreactivity against skin epitopes. To conclude, IgE autoantibodies and self-reactive T cells can contribute to the pathophysiology of AD based on the body of evidence in literature. However, many questions remain open. Future studies on autoreactivity in AD should especially focus on the clinical relevance, the contribution to the disease progression and chronicity on cellular level, the onset and therapeutic strategies.

/pdf/ige-autoantibodies-and-autoreactive-t-cells-and-their-role-2tvomyqtek.pdf

IgE autoantibodies and autoreactive T cells and their role in children and adults with atopic dermatitis.

Atopic dermatitis (AD), one of the most frequent inflammatory skin diseases worldwide, is believed to result from a disturbed skin barrier as well as aberrant immune reactions against per se harmless allergens. Starting mostly during childhood with a chronic, remitting relapsing course, the disease can persist into adulthood in about one fifth of patients. Immune reactions to self-proteins have been observed in AD patients already in the beginning of the Twentieth century, when human cellular extracts were shown to provoke skin lesions. However, the term "autoimmunity" has never been claimed, since AD is first and foremost an atopic disease. In contrast, this IgE-hallmarked autoreactivity was termed "autoallergy" and is ongoing discussed regarding its impact on the disease. Since severely affected patients tend to develop IgE-hypersensitivity reactions to numerous environmental allergens, the impact of immune responses to self-proteins is difficult to determine. On the other hand: any autoreactivity, irrespective of the magnitude, implicates the potential of driving the chronification of the disease while shaping the immune response. This review article revisits the observations made on autoallergy from an actual point of view and tries to approach the question whether these still point to a contribution to the disease.

/pdf/autoimmunity-or-not-in-atopic-dermatitis-1fk73s8i4v.pdf

Autoimmunity (or Not) in Atopic Dermatitis.

Atopiceczema/dermatitissyndrome(AEDS)isachronic,relapsing,multifactorialskinprocesswithaverycomplexinﬂammatory cascade (1–6). Many studies investigatedtheroleofimmunologic,physiologic,geneticparametersand the potential provoking factors, e.g. allergens,microbial factors, irritants, seasonal/climate changesand psychic stress in the pathogenesis of the disease(7–11).Theimpairedskinbarrier,sweatingfunctionandsweationcontentcanalsocontributetotheinductionofAEDS(4,5,12,13).Inaddition,mostoftheindividualswithAEDShaveapersonalorfamilyhistoryofallergicrhinitis, conjunctivitis or asthma with increased serumIgEantibodiesagainstinhalantorfoodallergens(extrin-sic, mixed type of AEDS). Some data were presentedabout the involvement of epithelial and sweat antigens(14, 15). Antinuclear antibodies were observed in ananimal model of atopic dermatitis (16) suggesting thatantibodiesofthenonallergictypealsocanbepresentinthe sera of patients with AEDS. Ambrozic et al. (17)found that in children younger than 3years of age(average age: 11months) the occurrence of antiphosp-holipid(APL)antibodieswaselevated.Inthisphenom-enontheyhypothesizedtheroleofnutritiveallergens.Inthisstudy,weanalysedtheassociationofallergen-speciﬁcantibodiesandtwoimportanttypesofAPL,nonallergic[anticardiolipin(ACL),anti-b

Association between the occurrence of the anticardiolipin IgM and mite allergen-specific IgE antibodies in children with extrinsic type of atopic eczema/dermatitis syndrome.

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Association between the occurrence of the anticardiolipin IgM and mite allergen-specific IgE antibodies in children with extrinsic type of atopic eczema/dermatitis syndrome.