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The Autoimmune Ecology

إيكولوجيا المناعة الذاتية
Authors: Juan‐Manuel Anaya; Carolina Ramírez‐Santana; Maria A. Alzate; Nicolás Molano‐González; Adriana Rojas‐Villarraga;

The Autoimmune Ecology

Abstract

Les maladies auto-immunes (MA) représentent un groupe hétérogène de troubles qui affectent des organes cibles spécifiques ou des systèmes d'organes multiples. Ces affections partagent des mécanismes immunopathogènes communs (c'est-à-dire la tautologie auto-immune), qui expliquent les similitudes cliniques qu'elles présentent entre elles ainsi que leur regroupement familial (c'est-à-dire la coagulation). Dans le cadre de la tautologie auto-immune, l'influence de l'exposition environnementale sur le risque de développer des MA est primordiale (c'est-à-dire l'écologie auto-immune). En fait, l'environnement, plus que la génétique, façonne le système immunitaire. L'écologie auto-immune s'apparente à l'exposome, c'est-à-dire à toutes les expositions - internes et externes - tout au long de la vie, interagissant avec des facteurs héréditaires (à la fois génétiques et épigénétiques) pour favoriser ou protéger contre l'auto-immunité et ses résultats. Nous présentons ici un aperçu de l'écologie auto-immune, en nous concentrant sur la réponse immunitaire aux agents environnementaux en général, et au microbiote, au tabagisme, à la consommation d'alcool et de café, au statut socio-économique (SSE), aux hormones de genre et de sexe, à la vitamine D, aux solvants organiques et aux vaccins en particulier. L'inclusion de l'écologie auto-immune dans l'étiologie et la santé des maladies améliorera la façon dont la médecine personnalisée est actuellement conçue et appliquée.

Las enfermedades autoinmunes (EA) representan un grupo heterogéneo de trastornos que afectan a órganos diana específicos o a múltiples sistemas de órganos. Estas afecciones comparten mecanismos inmunopatógenos comunes (es decir, la tautología autoinmune), que explican las similitudes clínicas que tienen entre ellas, así como su agrupación familiar (es decir, coagregación). Como parte de la tautología autoinmune, la influencia de la exposición ambiental en el riesgo de desarrollar EA es primordial (es decir, la ecología autoinmune). De hecho, el medio ambiente, más que la genética, da forma al sistema inmunológico. La ecología autoinmune es similar al exposoma, es decir, todas las exposiciones, internas y externas, a lo largo de la vida, que interactúan con factores hereditarios (tanto genéticos como epigenéticos) para favorecer o proteger contra la autoinmunidad y sus resultados. A continuación, proporcionamos una visión general de la ecología autoinmune, centrándonos en la respuesta inmune a los agentes ambientales en general, y la microbiota, el tabaquismo, el consumo de alcohol y café, el estado socioeconómico (ses), las hormonas sexuales y de género, la vitamina D, los disolventes orgánicos y las vacunas en particular. La inclusión de la ecología autoinmune en la etiología y la salud de la enfermedad mejorará la forma en que actualmente se concibe y aplica la medicina personalizada.

Autoimmune diseases (ADs) represent a heterogeneous group of disorders that affect specific target organs or multiple organ systems. These conditions share common immunopathogenic mechanisms (i.e., the autoimmune tautology), which explain the clinical similarities they have among them as well as their familial clustering (i.e., coaggregation). As part of the autoimmune tautology, the influence of environmental exposure on the risk of developing ADs is paramount (i.e., the autoimmune ecology). In fact, environment, more than genetics, shapes immune system. Autoimmune ecology is akin to exposome, that is all the exposures - internal and external - across the lifespan, interacting with hereditary factors (both genetics and epigenetics) to favor or protect against autoimmunity and its outcomes. Herein, we provide an overview of the autoimmune ecology, focusing on the immune response to environmental agents in general, and microbiota, cigarette smoking, alcohol and coffee consumption, socioeconomic status (SES), gender and sex hormones, vitamin D, organic solvents, and vaccines in particular. Inclusion of the autoimmune ecology in disease etiology and health will improve the way personalized medicine is currently conceived and applied.

تمثل أمراض المناعة الذاتية (ADs) مجموعة غير متجانسة من الاضطرابات التي تؤثر على أعضاء مستهدفة محددة أو أجهزة أعضاء متعددة. تشترك هذه الحالات في آليات مسببة للأمراض المناعية الشائعة (أي حشو المناعة الذاتية)، والتي تفسر أوجه التشابه السريرية بينها وكذلك تجميعها العائلي (أي التراكم). كجزء من حشو المناعة الذاتية، فإن تأثير التعرض البيئي على خطر الإصابة بـ ADs أمر بالغ الأهمية (أي بيئة المناعة الذاتية). في الواقع، البيئة، أكثر من علم الوراثة، تشكل الجهاز المناعي. بيئة المناعة الذاتية شبيهة بالفضائح، أي جميع التعرضات - الداخلية والخارجية - عبر العمر، والتفاعل مع العوامل الوراثية (كل من علم الوراثة وعلم الوراثة اللاجيني) لتفضيل أو الحماية من المناعة الذاتية ونتائجها. هنا، نقدم لمحة عامة عن بيئة المناعة الذاتية، مع التركيز على الاستجابة المناعية للعوامل البيئية بشكل عام، والميكروبات، وتدخين السجائر، واستهلاك الكحول والقهوة، والحالة الاجتماعية والاقتصادية (SES)، والجنس والهرمونات الجنسية، وفيتامين (د)، والمذيبات العضوية، واللقاحات على وجه الخصوص. سيؤدي إدراج بيئة المناعة الذاتية في مسببات الأمراض والصحة إلى تحسين الطريقة التي يتم بها حاليًا تصميم الطب الشخصي وتطبيقه.

Keywords

Radiology, Nuclear Medicine and Imaging, 2,3,7,8 tetrachlorodibenzo para dioxin, Prostaglandin, Immunological Mechanisms in Atherosclerosis Development, Interleukin 6, Autoimmunity, Review, Interleukin 8, Interleukin 1, Evolutionary ecology, Interleukin 2, Toll like receptor, Coffee, Gene, High mobility group b1 protein, Toll like receptor 9, Toll like receptor 8, Toll like receptor 7, Randomized controlled trial (topic), Immunoglobulin g, Autoimmune disease, T lymphocyte, Pathology, Alcohol consumption, Disease, Disease course, Genetics and Pathogenesis of Type 1 Diabetes, Innate immunity, Immunology and Microbiology, B lymphocyte activation, Ecology, Host (biology), Smoking, Toll like receptor 2, Life Sciences, Toll like receptor 1, personalized medicine, Toll like receptor 6, Toll like receptor 5, Toll like receptor 4, Toll like receptor 3, Clinical trial (topic), Organic solvent, Medicine, Epigenetics, ecology, Alcohol, Infection, environment, Human, Therapeutic Antibodies: Development, Engineering, and Applications, Dna methylation, Microflora, Immunology, polyautoimmunity, autoimmune disease, Environment, Systematic review (topic), Biochemistry, Genetics and Molecular Biology, Health Sciences, Genetics, Sex hormone, Immune response, Biology, Antibody, Tumor necrosis factor alpha, B cell activating factor, FOS: Clinical medicine, Gender, RC581-607, Environmental exposure, Nonhuman, Personalized medicine, Polyautoimmunity, Environmental factor, Social status, Interleukin 23, personalized medicine., Immune system, Immunoglobulin enhancer binding protein, Interleukin 27, FOS: Biological sciences, Meta analysis (topic), Gene expression, Risk factor, Vitamin d, Immunologic diseases. Allergy, Vaccine

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
85
Top 10%
Top 10%
Top 1%
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gold