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1.
Rheumatol Int ; 40(10): 1539-1554, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32666137

RESUMO

The coronavirus disease-2019 (COVID-19) pandemic is likely to pose new challenges to the rheumatology community in the near and distant future. Some of the challenges, like the severity of COVID-19 among patients on immunosuppressive agents, are predictable and are being evaluated with great care and effort across the globe. A few others, such as atypical manifestations of COVID-19 mimicking rheumatic musculoskeletal diseases (RMDs) are being reported. Like in many other viral infections, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection can potentially lead to an array of rheumatological and autoimmune manifestations by molecular mimicry (cross-reacting epitope between the virus and the host), bystander killing (virus-specific CD8 + T cells migrating to the target tissues and exerting cytotoxicity), epitope spreading, viral persistence (polyclonal activation due to the constant presence of viral antigens driving immune-mediated injury) and formation of neutrophil extracellular traps. In addition, the myriad of antiviral drugs presently being tried in the treatment of COVID-19 can result in several rheumatic musculoskeletal adverse effects. In this review, we have addressed the possible spectrum and mechanisms of various autoimmune and rheumatic musculoskeletal manifestations that can be precipitated by COVID-19 infection, its therapy, and the preventive strategies to contain the infection.


Assuntos
Doenças Autoimunes/fisiopatologia , Infecções por Coronavirus/fisiopatologia , Doenças Musculoesqueléticas/fisiopatologia , Pneumonia Viral/fisiopatologia , Doenças Reumáticas/fisiopatologia , Anticorpos Antinucleares/imunologia , Anticorpos Antifosfolipídeos/imunologia , Antivirais/efeitos adversos , Artralgia/etiologia , Artralgia/imunologia , Artralgia/fisiopatologia , Doenças Autoimunes/etiologia , Doenças Autoimunes/imunologia , Betacoronavirus , Transtornos da Coagulação Sanguínea/etiologia , Transtornos da Coagulação Sanguínea/imunologia , Transtornos da Coagulação Sanguínea/fisiopatologia , Infecções por Coronavirus/complicações , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/imunologia , Reações Cruzadas/imunologia , Armadilhas Extracelulares/imunologia , Produtos de Degradação da Fibrina e do Fibrinogênio , Síndrome de Guillain-Barré/etiologia , Síndrome de Guillain-Barré/imunologia , Síndrome de Guillain-Barré/fisiopatologia , Humanos , Inibidor de Coagulação do Lúpus/imunologia , Mimetismo Molecular , Síndrome de Linfonodos Mucocutâneos/etiologia , Síndrome de Linfonodos Mucocutâneos/imunologia , Síndrome de Linfonodos Mucocutâneos/fisiopatologia , Debilidade Muscular/etiologia , Debilidade Muscular/imunologia , Debilidade Muscular/fisiopatologia , Doenças Musculoesqueléticas/etiologia , Doenças Musculoesqueléticas/imunologia , Mialgia/etiologia , Mialgia/imunologia , Mialgia/fisiopatologia , Miocardite/etiologia , Miocardite/imunologia , Miocardite/fisiopatologia , Pandemias , Pneumonia Viral/complicações , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/imunologia , Doenças Reumáticas/etiologia , Doenças Reumáticas/imunologia
2.
Clin Immunol ; 217: 108480, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32461193

Assuntos
Autoanticorpos/imunologia , Autoantígenos/imunologia , Doenças Autoimunes/epidemiologia , Betacoronavirus/imunologia , Infecções por Coronavirus/epidemiologia , Proteínas do Nucleocapsídeo/imunologia , Pandemias , Pneumonia Viral/epidemiologia , Glicoproteína da Espícula de Coronavírus/imunologia , Anticorpos Antivirais/química , Anticorpos Antivirais/genética , Autoanticorpos/química , Autoanticorpos/genética , Autoantígenos/química , Autoantígenos/genética , Doenças Autoimunes/etiologia , Doenças Autoimunes/imunologia , Doenças Autoimunes/virologia , Autoimunidade , Betacoronavirus/patogenicidade , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/prevenção & controle , Infecções por Coronavirus/virologia , Reações Cruzadas , Expressão Gênica , Interações Hospedeiro-Patógeno/genética , Interações Hospedeiro-Patógeno/imunologia , Humanos , Imunidade Inata , Proteínas do Nucleocapsídeo/química , Proteínas do Nucleocapsídeo/genética , Pandemias/prevenção & controle , Pneumonia Viral/imunologia , Pneumonia Viral/prevenção & controle , Pneumonia Viral/virologia , Proteínas Associadas a Surfactantes Pulmonares/antagonistas & inibidores , Proteínas Associadas a Surfactantes Pulmonares/genética , Proteínas Associadas a Surfactantes Pulmonares/imunologia , Glicoproteína da Espícula de Coronavírus/química , Glicoproteína da Espícula de Coronavírus/genética , Vacinas Virais/efeitos adversos , Vacinas Virais/biossíntese
3.
Dermatol Online J ; 26(2)2020 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-32239891

RESUMO

Dermatomyositis is an auto-immune inflammatory myopathy that primarily affects the skin and muscle and can be triggered by exposure to various environmental factors. We present a patient with active syphilis infection who developed dermatomyositis and discuss the significance of anti-NXP2 autoantibody positivity.


Assuntos
Adenosina Trifosfatases/imunologia , Doenças Autoimunes/etiologia , Proteínas de Ligação a DNA/imunologia , Dermatomiosite/etiologia , Pele/patologia , Sífilis/complicações , Adulto , Autoanticorpos/sangue , Doenças Autoimunes/patologia , Dermatomiosite/imunologia , Dermatomiosite/patologia , Humanos , Masculino
6.
J Neuroimmunol ; 343: 577231, 2020 06 15.
Artigo em Inglês | MEDLINE | ID: mdl-32302793

RESUMO

Autoimmune limbic encephalitis is part of CASPR 2 antibody-associated disease. A man with this rare disorder and a very high antibody titre had a unique history of laboratory exposure to the antigen. Together with earlier observations this case calls for caution in laboratory handling of nerve tissue.


Assuntos
Doenças Autoimunes/etiologia , Doenças Autoimunes/imunologia , Encefalite Límbica/etiologia , Encefalite Límbica/imunologia , Pessoal de Laboratório Médico , Proteínas de Membrana/imunologia , Proteínas do Tecido Nervoso/imunologia , Exposição Ocupacional/efeitos adversos , Idoso , Autoanticorpos/imunologia , Autoantígenos/imunologia , Humanos , Masculino
7.
Sci Rep ; 10(1): 4509, 2020 03 11.
Artigo em Inglês | MEDLINE | ID: mdl-32161277

RESUMO

In several autoimmune diseases, e.g., pemphigoid disease (PD), autoantibodies are the direct cause of pathology. Albeit key requirements for antibody-mediated diseases were identified, their interactions and exact temporal and spatial interactions remained elusive. The skin is easily accessible for imaging. Thus, we selected epidermolysis bullosa acquisita (EBA), a PD with autoantibodies to type VII collagen (COL7), to visualize interactions of autoantibodies, target tissue and effector cells (neutrophils). Following injection into mice, anti-COL7 IgG bound to the dermal-epidermal junction (DEJ) within minutes. We unexpectedly observed an inhomogeneous distribution of autoantibodies along the DEJ. Thus, we hypothesized that specific external triggers may affect autoantibody distribution. Indeed, mechanical irritation led to an increased autoantibody binding along the DEJ. Subsequently, anti-COL7 IgG was injected into mice expressing green fluorescent protein under the LysM promoter (LysM-eGFP) mice. This allows to visualize myeloid cells in vivo in these animals. Using multiphoton imaging, we observed a limited extravasation of LysM-eGFP+ cells into skin was observed within 24 hours. Intriguingly, LysM-eGFP+ cells did not immediately co-localize with autoantibodies, which was only noted at later time points. Of note, interactions of LysM-eGFP+ with the autoantibodies at the DEJ were short-lived. Collectively, our results define the following checkpoints for autoantibody-induced tissue injury: (i) autoantibody egress to target tissue influenced by mechanical trigger factors, (ii) neutrophil recruitment into the vicinity of autoantibody deposits and (iii) short-term neutrophil localization to these deposits, as well as (iv) delayed recruitment of neutrophils with subsequent autoantibody-induced inflammation.


Assuntos
Autoanticorpos/imunologia , Suscetibilidade a Doenças/imunologia , Neutrófilos/imunologia , Animais , Doenças Autoimunes/etiologia , Doenças Autoimunes/metabolismo , Doenças Autoimunes/patologia , Biomarcadores , Biópsia , Colágeno Tipo VII/imunologia , Modelos Animais de Doenças , Imunofluorescência , Imunoglobulina G/imunologia , Camundongos , Neutrófilos/metabolismo , Pele/imunologia , Pele/metabolismo , Pele/patologia
8.
Environ Res ; 183: 109072, 2020 04.
Artigo em Inglês | MEDLINE | ID: mdl-32007747

RESUMO

BACKGROUND: Exposure to the environmental toxicant mercury (Hg) has been associated with immune dysregulation, including autoimmune disease, but few human studies have examined methylmercury (MeHg) exposure from fish consumption. OBJECTIVES: We examined associations between MeHg exposure and biological markers of autoimmunity and inflammation while adjusting for long chain polyunsaturated fatty acids (LCPUFA). METHOD: At age 19 years, hair total Hg (Y19Hg), LCPUFA status, a panel of 13 antinuclear antibodies (ANA), total serum immunoglobulins (Ig) IgG, IgA, and IgM and serum markers of inflammation (IL-1, IL-2, IL-6, IL-10, C-reactive protein (CRP), IFN-γ, TNF-α) were measured in the Seychelles Child Development Study (SCDS) Main Cohort (n = 497). Multivariable regression models investigated the association between Y19Hg and biomarkers, adjusting for prenatal total hair Hg (MatHg) and other relevant covariates, and with and without adjustment for LCPUFA. RESULTS: With each 1 ppm increase in Y19Hg (mean 10.23 (SD 6.02) ppm) we observed a 4% increased odds in a positive Combined ANA following adjustment for the n6:n3 LCPUFA ratio (ß = 0.036, 95%; CI: 0.001, 0.073). IgM was negatively associated with Y19Hg (ß = -0.016, 95%CI: 0.016, -0.002) in models adjusted for n-3, n-6 LCPUFA and when separately adjusted for the n-6:n-3 LCPUFA ratio. No associations were observed with MatHg. Total n-3 LCPUFA status was associated with reduced odds of a positive anti-ribonuclear protein (RNP) A. The n-3 LCPUFA were negatively associated with IL-6, IL-10, CRP, IFN-γ, TNF-α and positively with TNF-α:IL-10. There were positive associations between the n-6:n-3 ratio and IL-6, IL-10, CRP, IFN-γ, TNF-α and a negative association with TNF-α:IL-10. DISCUSSION: The Y19Hg exposure was associated with higher ANA and lower IgM albeit only following adjustment for the n-3 LCPUFA or the n-6:n-3 LCPUFA ratio. The clinical significance of these findings is unclear, but warrant follow up at an older age to determine any relationship to the onset of autoimmune disease.


Assuntos
Doenças Autoimunes , Ácidos Graxos Ômega-3 , Compostos de Metilmercúrio , Animais , Doenças Autoimunes/etiologia , Criança , Dieta , Ácidos Graxos Insaturados , Feminino , Humanos , Masculino , Compostos de Metilmercúrio/toxicidade , Gravidez , Seicheles , Adulto Jovem
9.
Clin Rev Allergy Immunol ; 58(2): 252-271, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32076943

RESUMO

Autoimmune liver diseases (AILDs) are potentially life-threatening chronic liver diseases which include autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis, and recently characterized IgG4-related sclerosing cholangitis. They are caused by immune attack on hepatocytes or bile ducts, with different mechanisms and clinical manifestations. The etiologies of AILDs include a susceptible genetic background, environment insults, infections, and changes of commensal microbiota, but remain complicated. Understanding of the underlying mechanisms of AILDs is mandatory for early diagnosis and intervention, which is of great importance for better prognosis. Thus, animal models are developed to mimic the pathogenesis, find biomarkers for early diagnosis, and for therapeutic attempts of AILDs. However, no animal models can fully recapitulate features of certain AILD, especially the late stages of diseases. Certain limitations include different living condition, cell composition, and time frame of disease development and resolution. Moreover, there is no IgG4 in rodents which exists in human. Nevertheless, the understanding and therapy of AILDs have been greatly advanced by the development and mechanistic investigation of animal models. This review will provide a comprehensive overview of traditional and new animal models that recapitulate different features and etiologies of distinct AILDs.


Assuntos
Doenças Autoimunes/etiologia , Doenças Autoimunes/metabolismo , Modelos Animais de Doenças , Hepatopatias/etiologia , Hepatopatias/metabolismo , Animais , Autoantígenos/imunologia , Doenças Autoimunes/diagnóstico , Autoimunidade , Biomarcadores , Diagnóstico Diferencial , Suscetibilidade a Doenças , Humanos , Imunoglobulina G/imunologia , Hepatopatias/diagnóstico , Camundongos Transgênicos , Prognóstico
10.
J Immunol Res ; 2020: 1438957, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32104714

RESUMO

The aim of this study was to examine the direct reaction of specific lectin/agglutinin antibodies to different tissue antigens to confirm the theory that reactivity between them may contribute to autoimmunities. Lectins are carbohydrate-binding proteins found in nearly all fruits and vegetables. Undigested lectins can penetrate the gut barriers, provoking an immune response that results in the production of antibodies against them. Using an enzyme-linked immunosorbent assay, we reacted lectin-specific antibodies with 62 different tissue antigens. Wheat germ agglutinin-specific antibody was the most reactive with the tissue antigens (37 tissues out of 62), followed by red kidney bean phytohemagglutinin-specific antibody (20), soybean agglutinin-specific antibody (20), and peanut agglutinin-specific antibody (15). This reaction between anti-lectin antibodies and many human tissue antigens may be due to possible molecular mimicry and cross-reactivity. After our results confirmed that anti-lectin antibodies bind with human tissues, we wanted to determine the prevalence of these antibodies in the blood of 500 nominally healthy donors. The percentage elevation of antibodies against different lectins ranged from 12 to 16% (Immunoglobulin G), 9.7-14.7% (Immunoglobulin A), 12-18% (Immunoglobulin M), and 7.8-14.6% (Immunoglobulin E). Serial dilutions and inhibition study confirmed that these reactions were specific. Finally, we tested the lectin-specific antibody level in sera both negative and positive for RF and ANA and found that IgM anti-lectin antibody levels were highly correlated with RF but not with ANA level. The reaction of anti-lectin antibodies with human tissue components and their detection in RF-positive samples may describe mechanisms by which the production of antibodies against undigested lectins may contribute to the pathogenesis of some autoimmune diseases.


Assuntos
Autoanticorpos/imunologia , Autoantígenos/imunologia , Autoimunidade , Lectinas/imunologia , Adolescente , Adulto , Idoso , Aglutininas/imunologia , Especificidade de Anticorpos/imunologia , Doenças Autoimunes/etiologia , Suscetibilidade a Doenças , Feminino , Humanos , Imunoglobulina G/imunologia , Imunoglobulina M/imunologia , Masculino , Pessoa de Meia-Idade , Ligação Proteica , Adulto Jovem
11.
Korean J Gastroenterol ; 75(1): 11-16, 2020 01 25.
Artigo em Coreano | MEDLINE | ID: mdl-31986568

RESUMO

Non-celiac gluten sensitivity (NCGS) is a term that is used to describe individuals who are not affected by celiac disease or wheat allergy, yet they have intestinal and/or extra-intestinal symptoms related to gluten ingestion with improvement of their symptoms upon withdrawing gluten from their diet. Gluten-related disorder groups are manifested by symptoms of gastrointestinal tract disorders, as well as hematological dermatological endocrinological, gynecological, rheumatological and nervous system symptoms. It is believed that NCGS represents heterogeneous groups with different subgroups characterized by different etiologies, clinical histories and clinical courses. There also appears to be an overlap between NCGS and irritable bowel syndrome (IBS). There is a need for establishing strict criteria for diagnosing NCGS. The absence of validated biomarkers remains a significant limitation for research studies on NCGS. New evidence shows that a gluten-free diet may be beneficial for some patients with gastrointestinal symptoms, such as those symptoms commonly found in patients with IBS. Further studies about NCGS are needed.


Assuntos
Gastroenteropatias/diagnóstico , Glutens/efeitos adversos , Dor Abdominal/diagnóstico , Dor Abdominal/etiologia , Doenças Autoimunes/diagnóstico , Doenças Autoimunes/etiologia , Dieta Livre de Glúten , Hipersensibilidade Alimentar/diagnóstico , Hipersensibilidade Alimentar/etiologia , Gastroenteropatias/etiologia , Glutens/administração & dosagem , Síndrome do Intestino Irritável/diagnóstico , Síndrome do Intestino Irritável/etiologia
13.
Arthritis Rheumatol ; 72(2): 359-370, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31464028

RESUMO

OBJECTIVE: Patients with hypomorphic mutations in DNase II develop a severe and debilitating autoinflammatory disease. This study was undertaken to compare the disease parameters in these patients to those in a murine model of DNase II deficiency, and to evaluate the role of specific nucleic acid sensors and identify the cell types responsible for driving the autoinflammatory response. METHODS: To avoid embryonic death, Dnase2-/- mice were intercrossed with mice that lacked the type I interferon (IFN) receptor (Ifnar-/- ). The hematologic changes and immune status of these mice were evaluated using complete blood cell counts, flow cytometry, serum cytokine enzyme-linked immunosorbent assays, and liver histology. Effector cell activity was determined by transferring T cells from Dnase2-/- × Ifnar-/- double-knockout (DKO) mice into Rag1-/- mice, and 4 weeks after cell transfer, induced changes were assessed in the recipient mice. RESULTS: In Dnase2-/- × Ifnar-/- DKO mice, many of the disease features found in DNase II-deficient patients were recapitulated, including cytopenia, extramedullary hematopoiesis, and liver fibrosis. Dnase2+/+ × Rag1-/- mice (n > 22) developed a hematologic disorder that was attributed to the transfer of an unusual IFNγ-producing T cell subset from the spleens of donor Dnase2-/- × Ifnar-/- DKO mice. Autoinflammation in this murine model did not depend on the stimulator of IFN genes (STING) pathway but was highly dependent on the chaperone protein Unc93B1. CONCLUSION: Dnase2-/- × Ifnar-/- DKO mice may be a valid model for exploring the innate and adaptive immune mechanisms responsible for the autoinflammation similar to that seen in DNASE2-hypomorphic patients. In this murine model, IFNγ is required for T cell activation and the development of clinical manifestations. The role of IFNγ in DNASE2-deficient patient populations remains to be determined, but the ability of Dnase2-/- mouse T cells to transfer disease to Rag1-/- mice suggests that T cells may be a relevant therapeutic target in patients with IFN-related systemic autoinflammatory diseases.


Assuntos
Doenças Autoimunes/etiologia , Endodesoxirribonucleases/deficiência , Inflamação/imunologia , Interferon gama/biossíntese , Células Th1/metabolismo , Animais , Modelos Animais de Doenças , Interferon Tipo I , Camundongos , Camundongos Endogâmicos C57BL
15.
Occup Environ Med ; 77(2): 64-69, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31848232

RESUMO

OBJECTIVES: Increased risk has been suggested for autoimmune rheumatic diseases following solvent exposure. The evidence for specific solvents is limited, and little is known about exposure-response relations. Styrene is an aromatic, organic solvent and the objective of this study was to analyse the association between occupational styrene exposure and autoimmune rheumatic diseases in men and women. METHODS: We followed 72 212 styrene-exposed workers of the Danish reinforced plastics industry from 1979 to 2012. We modelled full work history of styrene exposure from employment history, survey data and historical styrene exposure measurements. We identified cases in the national patient registry and investigated gender-specific exposure-response relations by cumulative styrene exposure for different exposure time windows adjusting for age, calendar year and educational level. RESULTS: During 1 515 126 person-years of follow-up, we identified 718 cases of an autoimmune rheumatic disease, of which 73% were rheumatoid arthritis. When adjusting for potential confounders and comparing the highest with the lowest styrene exposure tertile, we observed a statistically non-significantly increased risk of systemic sclerosis among women (incidence rate ratio (IRR)=2.50; 95% CI 0.50 to 12.50) and men (IRR=1.86; 95 % CI 0.50 to 7.00), based on 9 and 22 cases, respectively. Results were inconsistent for the other autoimmune rheumatic diseases examined. CONCLUSION: This study suggests an association between occupational styrene exposure and systemic sclerosis in men as well as in women but based on few cases. This is a new finding and has to be replicated before conclusions can be drawn.


Assuntos
Doenças Autoimunes/etiologia , Doenças Profissionais/etiologia , Exposição Ocupacional/efeitos adversos , Doenças Reumáticas/etiologia , Escleroderma Sistêmico/etiologia , Solventes/efeitos adversos , Estireno/efeitos adversos , Adulto , Idoso , Artrite Reumatoide/epidemiologia , Artrite Reumatoide/etiologia , Doenças Autoimunes/epidemiologia , Dinamarca/epidemiologia , Humanos , Indústria Manufatureira , Pessoa de Meia-Idade , Doenças Profissionais/epidemiologia , Plásticos , Sistema de Registros , Doenças Reumáticas/epidemiologia , Escleroderma Sistêmico/epidemiologia , Fatores Sexuais
16.
Autoimmun Rev ; 19(1): 102422, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31733369

RESUMO

Paraneoplastic autoimmune disorders (PAD) represent a group of autoimmune diseases associated with neoplasms. As a consequence of a remote autoimmunity-mediated effect, PAD are found in multiple organs or tissues, including the skin, blood and nervous system. Compared with non-paraneoplastic autoimmune diseases, PAD have different aetiologies, pathologies, disease symptoms and treatment responses. There are two main origins of autoimmunity in PAD: neoplasm-mediated dysregulated homeostasis in immune cells/organs and in autoantigens. Pathologically, PAD are mediated predominantly by either autoantibodies or autoreactive T-cells. In the past decade, significant progress has been achieved in increasing our understanding of the aetiology and pathology of PAD. In this review article, we aim to provide a comprehensive overview of the recent advances in this field.


Assuntos
Doenças Autoimunes/etiologia , Doenças Autoimunes/fisiopatologia , Neoplasias/fisiopatologia , Autoanticorpos , Autoantígenos , Humanos
17.
Best Pract Res Clin Endocrinol Metab ; 34(1): 101373, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-31864909

RESUMO

The association between autoimmune atrophic gastritis and thyroid disorders has been observed since the early 1960s and the expression "thyrogastric syndrome" was coined to indicate the presence of thyroid autoantibodies or autoimmune thyroid disease in patients with pernicious anemia, a late clinical stage of autoimmune atrophic gastritis. More recently, it was confirmed that autoimmune thyroid disorders, in particular Hashimoto's thyroiditis, may be frequently associated with other organ-specific, immune-mediated disorders, such as autoimmune atrophic gastritis or celiac disease. The association of Hashimoto's thyroiditis with autoimmune atrophic gastritis or celiac disease in adult patients is currently considered part of the polyglandular autoimmune syndromes which include several autoimmune disorders associated with an autoaggressive impairment of endocrine glands. From a clinical point of view, the thyro-entero-gastric autoimmunity may lead to potentially serious consequences like anemia, micronutrients deficiencies, and drugs malabsorption, as well as to an increased risk for malignancies. These alterations may frequently present in an underhand manner, with consequent diagnostic and treatment delays. Many aspects of the association between thyroid, gastric and intestinal autoimmune diseases still await clarification. The present review focuses on the embryological, genetic and pathophysiological aspects of thyro-entero-gastric autoimmunity. In particular, the current diagnostic criteria of autoimmune thyroid disease, autoimmune atrophic gastritis, and celiac disease are reviewed, along with the evidences for their association in poly-autoimmunity syndromes. The benefits of proactive screening of autoimmune thyroid disorders in patients with autoimmune gastritis or enteropathy and viceversa are also discussed.


Assuntos
Doenças Autoimunes/etiologia , Doenças Autoimunes/terapia , Gastrite/terapia , Enteropatias/terapia , Tireoidite Autoimune/terapia , Adulto , Autoimunidade/fisiologia , Gastrite/complicações , Gastrite/etiologia , Gastrite/imunologia , Humanos , Enteropatias/etiologia , Enteropatias/imunologia , Enteropatias/patologia , Poliendocrinopatias Autoimunes/etiologia , Poliendocrinopatias Autoimunes/imunologia , Poliendocrinopatias Autoimunes/terapia , Tireoidite Autoimune/etiologia , Tireoidite Autoimune/imunologia , Tireoidite Autoimune/patologia
18.
Nat Med ; 25(12): 1822-1832, 2019 12.
Artigo em Inglês | MEDLINE | ID: mdl-31806905

RESUMO

Although intermittent increases in inflammation are critical for survival during physical injury and infection, recent research has revealed that certain social, environmental and lifestyle factors can promote systemic chronic inflammation (SCI) that can, in turn, lead to several diseases that collectively represent the leading causes of disability and mortality worldwide, such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders. In the present Perspective we describe the multi-level mechanisms underlying SCI and several risk factors that promote this health-damaging phenotype, including infections, physical inactivity, poor diet, environmental and industrial toxicants and psychological stress. Furthermore, we suggest potential strategies for advancing the early diagnosis, prevention and treatment of SCI.


Assuntos
Doença Crônica/epidemiologia , Inflamação/fisiopatologia , Longevidade/genética , Doenças Autoimunes/etiologia , Doenças Autoimunes/fisiopatologia , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/fisiopatologia , Diabetes Mellitus/etiologia , Diabetes Mellitus/fisiopatologia , Humanos , Inflamação/complicações , Inflamação/epidemiologia , Estilo de Vida , Longevidade/fisiologia , Neoplasias/etiologia , Neoplasias/fisiopatologia , Doenças Neurodegenerativas/etiologia , Doenças Neurodegenerativas/fisiopatologia , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatia Gordurosa não Alcoólica/fisiopatologia , Insuficiência Renal Crônica/etiologia , Insuficiência Renal Crônica/fisiopatologia , Fatores de Risco
19.
J Immunol Res ; 2019: 8380214, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31886311

RESUMO

Anticardiolipin antibody (ACA) is a kind of autoantibody and is one of the antiphospholipid antibodies (aPLs). Phospholipids with a negative charge on platelets and endothelial cell membranes are ACA target antigens. ACA is common in systemic lupus erythematosus and other autoimmune diseases and is closely associated with thrombosis, thrombocytopenia, and spontaneous abortion. In 1983, Harris established a method for detecting ACA, and research on the antibody has gained worldwide attention and has developed rapidly. For this review, we browsed articles that cover most of the ACA-related studies in the last 25 years and extracted influential ideas and conclusions in this field.


Assuntos
Anticorpos Anticardiolipina/imunologia , Autoantígenos/imunologia , Doenças Autoimunes/etiologia , Cardiolipinas/imunologia , Suscetibilidade a Doenças , Pesquisa , Doenças Autoimunes/diagnóstico , Doenças Autoimunes/metabolismo , Biomarcadores , Gerenciamento Clínico , Humanos
20.
J Immunol Res ; 2019: 7592851, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31886309

RESUMO

A protein undergoes many types of posttranslation modification. Citrullination is one of these modifications, where an arginine amino acid is converted to a citrulline amino acid. This process depends on catalytic enzymes such as peptidylarginine deiminase enzymes (PADs). This modification leads to a charge shift, which affects the protein structure, protein-protein interactions, and hydrogen bond formation, and it may cause protein denaturation. The irreversible citrullination reaction is not limited to a specific protein, cell, or tissue. It can target a wide range of proteins in the cell membrane, cytoplasm, nucleus, and mitochondria. Citrullination is a normal reaction during cell death. Apoptosis is normally accompanied with a clearance process via scavenger cells. A defect in the clearance system either in terms of efficiency or capacity may occur due to massive cell death, which may result in the accumulation and leakage of PAD enzymes and the citrullinated peptide from the necrotized cell which could be recognized by the immune system, where the immunological tolerance will be avoided and the autoimmune disorders will be subsequently triggered. The induction of autoimmune responses, autoantibody production, and cytokines involved in the major autoimmune diseases will be discussed.


Assuntos
Doenças Autoimunes/etiologia , Doenças Autoimunes/metabolismo , Citrulina/metabolismo , Suscetibilidade a Doenças , Desiminases de Arginina em Proteínas/metabolismo , Doenças Autoimunes/diagnóstico , Autoimunidade , Biomarcadores , Citrulinação , Predisposição Genética para Doença , Humanos , Desiminases de Arginina em Proteínas/genética , Fatores de Risco
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