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1.
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
2.
Brain Nerve ; 71(9): 1003-1012, 2019 Sep.
Artigo em Japonês | MEDLINE | ID: mdl-31506402

RESUMO

We present a case of a 73-year-old female who developed subacute memory disturbance, reduced consciousness and quadriparesis following pernicious anemia. Brain magnetic resonance imagings (MRI) in diffusion weighted, T2 weighted and fluid attenuated inversion recovery (FLAIR) images revealed hyperintensities in bilateral frontal, parietal, temporal and occipital cortices, left thalamus, bilateral splenium of corpus callosum, and bilateral subcortical white matters. Brain gadolinium enhanced T1 weighted MRI revealed very slight post-contrast enhancement lesions in the right posterior temporal region and bilateral parietal regions. Serum was negative for anti- aquaporin (AQP) 4 antibody, anti-glutamic acid decarboxylase (GAD) antibody and anti-voltage-gated potassium channel (VGKC) antibody, and cerebrospinal fluid (CSF) was negative for anti- N-methyl-D-aspartate (NMDA) receptor antibody. CSF analysis showed slight protein elevation with normal cellular content. No evidence of neoplasm was observed using whole-body 18 F -fluorodeoxyglucose- positron emission tomography/computed tomography. Pathological findings of the left frontal lesion revealed perivascular and scattered parechymal T-lymphocytic infiltration, and astrogliosis without vascular hyalinization. Patient achieved partial recovery during two intraveneous pulse methylprednisolone treatments, and exacerbation afterwards. After the third intraveneous pulse methylprednisolone treatment, remission is sustained for six years. This case can be regarded as autoantibody-negative but probable autoimmune encephalitis with the features of nonparaneoplastic panencephalitis and treatable dementia. Nonparaneoplastic autoimmune panencephalitis with widespread multifocal brain lesions on brain MRI is extremely rare, with exception of anti- NMDA receptor antibody encephalitis.


Assuntos
Anemia Perniciosa/complicações , Doenças Autoimunes/etiologia , Demência/etiologia , Encefalite/etiologia , Idoso , Doenças Autoimunes/tratamento farmacológico , Encéfalo/diagnóstico por imagem , Encéfalo/patologia , Demência/tratamento farmacológico , Encefalite/tratamento farmacológico , Feminino , Seguimentos , Humanos , Imagem por Ressonância Magnética
3.
Int J Mol Sci ; 20(18)2019 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-31540175

RESUMO

The oral cavity is suggested as the reservoir of bacterial infection, and the oral and pharyngeal biofilms formed by oral bacterial flora, which is comprised of over 700 microbial species, have been found to be associated with systemic conditions. Almost all oral microorganisms are non-pathogenic opportunistic commensals to maintain oral health condition and defend against pathogenic microorganisms. However, oral Streptococci, the first microorganisms to colonize oral surfaces and the dominant microorganisms in the human mouth, has recently gained attention as the pathogens of various systemic diseases, such as infective endocarditis, purulent infections, brain hemorrhage, intestinal inflammation, and autoimmune diseases, as well as bacteremia. As pathogenic factors from oral Streptococci, extracellular polymeric substances, toxins, proteins and nucleic acids as well as vesicles, which secrete these components outside of bacterial cells in biofilm, have been reported. Therefore, it is necessary to consider that the relevance of these pathogenic factors to systemic diseases and also vaccine candidates to protect infectious diseases caused by Streptococci. This review article focuses on the mechanistic links among pathogenic factors from oral Streptococci, inflammation, and systemic diseases to provide the current understanding of oral biofilm infections based on biofilm and widespread systemic diseases.


Assuntos
Estomatite/microbiologia , Infecções Estreptocócicas/microbiologia , Streptococcus/fisiologia , Idoso , Doenças Autoimunes/etiologia , Autoimunidade , Aderência Bacteriana , Biofilmes , Biomarcadores , Proteínas de Ligação a DNA/metabolismo , Humanos , Masculino , Estomatite/diagnóstico , Infecções Estreptocócicas/diagnóstico , Virulência , Fatores de Virulência
4.
Life Sci ; 233: 116744, 2019 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-31401314

RESUMO

The prevalence of autoimmune diseases (ADs) has increased over the past few decades. Vitamin D deficiency is a common factor in many of these diseases, whose etiology remains poorly understood. The objective of this study was to review published data on the role of vitamin D in ADs. Vitamin D insufficiency has been described as an important factor in the development of some ADs, generally attributed to the key role of this vitamin in the immune system. Most studies show that adequate supplementation can prevent and improve the development of some of these diseases, although the optimal vitamin D dose remains controversial. We highlight the importance of measuring serum vitamin D levels of the population and developing strategies to improve and maintain levels with no health risks.


Assuntos
Doenças Autoimunes/prevenção & controle , Suplementos Nutricionais , Deficiência de Vitamina D/complicações , Vitamina D/sangue , Vitaminas/sangue , Doenças Autoimunes/etiologia , Humanos , Vitamina D/administração & dosagem , Vitaminas/administração & dosagem
5.
Acta Diabetol ; 56(12): 1239-1245, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31423559

RESUMO

Immune checkpoint inhibitors (CPI) are increasingly being used in oncology, and many autoimmune side effects have been described. Diabetes mellitus (DM) has been reported in approximately 1% of subjects treated with programmed cell death-1 and programmed death ligand 1 (PD-1/PD-L1) inhibitors, alone or in association with CTLA-4 inhibitors. In the present mini-review, we aimed to describe different clinical pictures and pathophysiology associated with these forms of diabetes. Data on CPI-related DM was gathered from the largest case series in the literature and from our centre dedicated to immunotherapy complications (ImmuCare-Hospices Civils de Lyon). Most cases are acute autoimmune insulin-dependent diabetes which are similar to fulminant diabetes (extremely acute onset with concomitant near-normal HbA1c levels). Other cases, however, have a phenotype close to type 2 diabetes or appear as a decompensation of previously known type 2 diabetes. The occurrence of diabetes can also be a complication of autoimmune pancreatitis induced by CPI use. Finally, two cases of diabetes in a context of autoimmune lipoatrophy have recently been described. Regarding the wide variety of CPI-induced diabetes, the discovery of a glucose disorder under CPI should motivate specialised care for aetiological diagnosis and appropriate treatment.


Assuntos
Pontos de Checagem do Ciclo Celular , Diabetes Mellitus Tipo 2/induzido quimicamente , Imunoterapia/efeitos adversos , Inibidores de Proteínas Quinases/efeitos adversos , Doenças Autoimunes/induzido quimicamente , Doenças Autoimunes/epidemiologia , Doenças Autoimunes/etiologia , Antígeno B7-H1/antagonistas & inibidores , Antígeno B7-H1/imunologia , Antígeno CTLA-4/antagonistas & inibidores , Antígeno CTLA-4/imunologia , Pontos de Checagem do Ciclo Celular/efeitos dos fármacos , Pontos de Checagem do Ciclo Celular/imunologia , Diabetes Mellitus Lipoatrófica/induzido quimicamente , Diabetes Mellitus Lipoatrófica/epidemiologia , Diabetes Mellitus Lipoatrófica/imunologia , Diabetes Mellitus Tipo 1/induzido quimicamente , Diabetes Mellitus Tipo 1/complicações , Diabetes Mellitus Tipo 1/diagnóstico , Diabetes Mellitus Tipo 1/epidemiologia , Diabetes Mellitus Tipo 2/diagnóstico , Diabetes Mellitus Tipo 2/epidemiologia , Diabetes Mellitus Tipo 2/imunologia , Humanos , Inibidores de Proteínas Quinases/uso terapêutico
6.
BMJ Case Rep ; 12(8)2019 Aug 02.
Artigo em Inglês | MEDLINE | ID: mdl-31377716

RESUMO

Thymoma-associated multiorgan autoimmunity is a relatively new term to describe the rare paraneoplastic syndrome that complicates thymoma, which can involve the thyroid, liver and intestine in addition to the skin. The pathology often indicates a graft-versus-host-like pattern commonly observed in recipients of an allogeneic haematopoietic cell transplant. We report a case of type B2 and B3 thymoma with invasion to the lung and pleura in a patient who presented with oral lichen planus and graft-versus-host-like erythroderma. The cutaneous lesions improved after complete resection of the thymoma in combination with systemic glucocorticoids, which was subsequently complicated by cytomegalovirus pneumonitis.


Assuntos
Doenças Autoimunes/tratamento farmacológico , Glucocorticoides/uso terapêutico , Timoma/cirurgia , Neoplasias do Timo/cirurgia , Doenças Autoimunes/etiologia , Terapia Combinada , Glucocorticoides/efeitos adversos , Humanos , Biópsia Guiada por Imagem , Líquen Plano Bucal/etiologia , Pulmão/diagnóstico por imagem , Pulmão/patologia , Masculino , Pessoa de Meia-Idade , Invasividade Neoplásica , Pleura/patologia , Timoma/complicações , Timoma/patologia , Neoplasias do Timo/complicações , Neoplasias do Timo/patologia
7.
Autoimmun Rev ; 18(9): 102350, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31323357

RESUMO

Vitamin D plays a key role in in calcium homeostasis and, thus, provides an important support in bone growth by aiding in the mineralization of the collagen matrix. However, vitamin D performs various immunomodulatory, anti-inflammatory, antioxidant and anti-fibrotic actions. Autoimmune diseases result from an aberrant activation of the immune system, whereby the immune response is directed against harmless self-antigens. Does vitamin D play a role in the pathophysiology of autoimmune diseases? And, if so, what is its role? In the last decade, researchers' interest in vitamin D and its correlations with autoimmune diseases has considerably increased. We conducted a literature review, covering the period January 1, 2009 through March 30, 2019, in PubMed. We analyzed more than 130 studies in order to find a correlation between vitamin D levels and its effect upon several autoimmune diseases. The analysis demonstrated an inverse association between vitamin D and the development of several autoimmune diseases, such as SLE, thyrotoxicosis, type 1 DM, MS, iridocyclitis, Crohn's disease, ulcerative colitis, psoriasis vulgaris, seropositive RA, polymyalgia rheumatica. International multicenter study could allow us to confirm the data already present in the literature in the single clinical studies and to evaluate when to effectively supplement vitamin D in patients who do not take corticosteroids.


Assuntos
Doenças Autoimunes/etiologia , Doenças Autoimunes/terapia , Vitamina D/fisiologia , Doenças Autoimunes/sangue , Doenças Autoimunes/epidemiologia , Comorbidade , Suplementos Nutricionais , Prática Clínica Baseada em Evidências/tendências , Humanos , Sistema Imunitário/efeitos dos fármacos , Vitamina D/farmacologia , Vitamina D/uso terapêutico , Deficiência de Vitamina D/complicações , Deficiência de Vitamina D/tratamento farmacológico , Deficiência de Vitamina D/epidemiologia , Deficiência de Vitamina D/imunologia
9.
Nutrients ; 11(5)2019 May 05.
Artigo em Inglês | MEDLINE | ID: mdl-31060286

RESUMO

The incidence and prevalence of autoimmune diseases have increased in Western countries over the last years. The pathogenesis of these disorders is multifactorial, with a combination of genetic and environmental factors involved. Since the epidemiological changes cannot be related to genetic background, which did not change significantly in that time, the role of environmental factors has been reconsidered. Among these, dietary habits, and especially an excessive salt, typical of processed foods, has been implicated in the development of autoimmune diseases. In this review, we summarize current evidence, deriving both from experimental models and clinical studies, on the capability of excessive salt intake to exacerbate proinflammatory responses affecting the pathogenesis of immune-mediated diseases. Data on several diseases are presented, including rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, and Crohn's disease, with many of them supporting a proinflammatory effect of salt. Likewise, a hypertonic microenvironment showed similar effects in experimental models both in vivo and in vitro. However, murine models of spontaneous autoimmune polyneuropathy exposed to high salt diet suggest opposite outcomes. These results dictate the need to further analyse the role of cooking salt in the treatment and prevention of autoimmune diseases, trying to shape a fine tuning between the possible advantages of a restricted salt intake and the changes in circulating metabolites, mediators, and hormones which come along salt consumption and could in turn influence autoimmunity.


Assuntos
Doenças Autoimunes/etiologia , Comportamento Alimentar , Análise de Alimentos , Cloreto de Sódio na Dieta/administração & dosagem , Cloreto de Sódio na Dieta/efeitos adversos , Cloreto de Sódio/efeitos adversos , Animais , Relação Dose-Resposta a Droga , Humanos , Cloreto de Sódio/administração & dosagem
10.
J Pediatr Endocrinol Metab ; 32(5): 479-488, 2019 May 27.
Artigo em Inglês | MEDLINE | ID: mdl-31075085

RESUMO

Background Females with Turner syndrome (TS) are prone to develop autoimmune diseases (AIDs). The X chromosome contains several immune-related genes. Growth hormone (GH) and estrogens modulate the immune system. We aimed to clarify whether the loss of a specific X chromosome gene locus and the administration of GH and estradiol facilitate the development of AIDs in TS females. Methods Retrospective data on clinical course, AIDs, karyotype and treatment were analyzed from a cohort of 286 Czech females with TS (current age 2.8-43.3 years; median age 18.7 years). The karyotypes were sorted using two different classification systems: a mosaicism-focused and an isochromosome (isoXq)-focused approach. Karyotype subgroups with a significantly higher prevalence of AIDs were further evaluated. Data of common therapies were correlated with the prevalence of AIDs. Results The most frequent AIDs were autoimmune thyroid disease (AITD; 37.4%; n = 107) and celiac disease (CD; 8.7%; n = 25). All karyotype subgroups were prone to develop AIDs. Females with an isolated Xp deletion had a significantly higher prevalence of AITD and CD compared to all other individuals with TS (AITD: 66.0% vs. 31.5%, p < 0.0001; CD: 17.4% vs. 7.2%; p = 0.04, respectively). We observed no link between the mean age at initiation as well as the duration of GH and/or estrogen administration and the occurrence of AIDs. Conclusions Isolated Xp deletion contributes to the development of AIDs in TS patients. The haploinsufficiency of genes located in Xpter-p11.2 may explain this observation. Common therapies used in TS do not modify the risk of AIDs.


Assuntos
Doenças Autoimunes/etiologia , Deleção Cromossômica , Cromossomos Humanos X/genética , Síndrome de Turner/genética , Adolescente , Adulto , Doenças Autoimunes/epidemiologia , Criança , Pré-Escolar , República Tcheca/epidemiologia , Feminino , Seguimentos , Humanos , Cariotipagem , Prevalência , Prognóstico , Estudos Retrospectivos , Síndrome de Turner/complicações , Adulto Jovem
11.
Int J Mol Sci ; 20(10)2019 May 24.
Artigo em Inglês | MEDLINE | ID: mdl-31137683

RESUMO

Immune checkpoint inhibitors block the checkpoint molecules. Different types of cancer immune checkpoint inhibitors have been approved recently: CTLA-4 monoclonal antibodies (as ipilimumab); anti-PD-1 monoclonal antibodies (as pembrolizumab and nivolumab); and anti-PD-L1 monoclonal antibodies (as atezolizumab, avelumab, and durmalumab). We collect recent published results about autoimmune endocrine dysfunctions associated with cancer antibody immunotherapies. These agents cause a raised immune response leading to immune-related adverse events (irAEs), varying from mild to fatal, based on the organ system and severity. Immune-related endocrine toxicities are usually irreversible in 50% of cases, and include hypophysitis, thyroid dysfunctions, type 1 diabetes mellitus, and adrenal insufficiency. Anti-PD-1-antibodies are more frequently associated with thyroid dysfunctions (including painless thyroiditis, hypothyroidism, thyrotoxicosis, or thyroid storm), while the most frequent irAE related to anti-CTLA-4-antibodies is hypophysitis. The combination of anti-CTLA-4 and anti-PD-1 antibodies is associated with a 30% chance of irAEs. Symptoms and clinical signs vary depending on the target organ. IrAEs are usually managed by an oncological therapist, but in more challenging circumstances (i.e., for new onset insulin-dependent diabetes, hypoadrenalism, gonadal hormones dysfunctions, or durable hypophysitis) an endocrinologist is needed.


Assuntos
Doenças Autoimunes/etiologia , Doenças do Sistema Endócrino/etiologia , Imunoterapia/efeitos adversos , Neoplasias/terapia , Animais , Anticorpos Monoclonais/efeitos adversos , Antineoplásicos/efeitos adversos , Humanos
12.
Acta Oncol ; 58(8): 1170-1177, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31131659

RESUMO

Background: Patients with certain autoimmune diseases (AID) have an increased risk of developing diffuse large B-cell lymphoma (DLBCL). However, the occurrence of AID in patients with DLBCL as well as the impact of AID on outcome has not been extensively studied. The main purpose of this study was to establish the occurrence of AIDs in a population-based cohort of DLBCL patients and to compare outcomes in patients with or without AID treated with rituximab(R)-CHOP/CHOP-like treatment. We also aimed to analyse gender differences and the potential role of different AIDs on outcome and the frequency of treatment-associated neutropenic fever. Patients and methods: All adult patients treated 2000-2013 with R-CHOP/CHOP-like treatment for DLBCL in four counties of Sweden were included (n = 612). Lymphoma characteristics, outcome and the presence of AID were obtained through medical records. Results: The number of patients with AID was 106 (17.3%). Thyroid disease dominated (n = 33, 31.1%) followed by rheumatoid arthritis (RA) (n = 24, 22.6%). The proportion of AID was significantly higher in females (59/254, 23.2%) vs. in males (47/358, 13.1%) (p = .001). In the whole cohort there was no difference in event free survival (EFS) or overall survival (OS) between patients with or without AID. However, patients with an AID primarily mediated by B-cell responses (thyroid disorders excluded) had a worse OS (p = .037), which seemed to affect only women. The AID group more often had neutropenic fever after first treatment (16.0% vs 8.7%, p = .034) and those with neutropenic fever had a worse OS (p = .026) in Kaplan-Meier analyses. Conclusion: There is a high prevalence of AID among patients with DLBCL. AIDs categorized as primarily B-cell mediated (in this study mainly RA, systemic lupus erythematosus and Sjögren's syndrome) may be associated with inferior OS. AID patients may be more prone to neutropenic fever compared to patients without concomitant AID.


Assuntos
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem , Doenças Autoimunes/epidemiologia , Neutropenia Febril Induzida por Quimioterapia/epidemiologia , Linfoma Difuso de Grandes Células B/complicações , Rituximab/administração & dosagem , Adulto , Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos , Doenças Autoimunes/etiologia , Linfócitos B/imunologia , Neutropenia Febril Induzida por Quimioterapia/etiologia , Ciclofosfamida/administração & dosagem , Ciclofosfamida/efeitos adversos , Intervalo Livre de Doença , Doxorrubicina/administração & dosagem , Doxorrubicina/efeitos adversos , Feminino , Humanos , Linfoma Difuso de Grandes Células B/tratamento farmacológico , Linfoma Difuso de Grandes Células B/mortalidade , Masculino , Prednisona/administração & dosagem , Prednisona/efeitos adversos , Prevalência , Estudos Retrospectivos , Rituximab/efeitos adversos , Fatores Sexuais , Análise de Sobrevida , Suécia/epidemiologia , Linfócitos T/imunologia , Vincristina/administração & dosagem , Vincristina/efeitos adversos , Adulto Jovem
13.
Crit Rev Microbiol ; 45(4): 394-412, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31145640

RESUMO

The exact aetiology of most autoimmune diseases remains unknown, nonetheless, several factors contributing to the induction or exacerbation of autoimmune reactions have been suggested. These include the genetic profile and lifestyle of the affected individual in addition to environmental triggers such as bacterial, parasitic, fungal and viral infections. Infections caused by viruses usually trigger a potent immune response that is necessary for the containment of the infection; however, in some cases, a failure in the regulation of this immune response may lead to harmful immune reactions directed against the host's antigens. The autoimmune attack can be carried out by different arms and components of the immune system and through different possible mechanisms including molecular mimicry, bystander activation, and epitope spreading among others. In this review, we examine the data available for the involvement of viral infections in triggering or exacerbating autoimmune diseases in addition to discussing the mechanisms by which these viral infections and the immune pathways they trigger possibly contribute to the development of autoimmunity.


Assuntos
Doenças Autoimunes/etiologia , Doenças Autoimunes/fisiopatologia , Interações Hospedeiro-Patógeno , Viroses/complicações , Viroses/patologia , Animais , Modelos Animais de Doenças , Humanos
14.
EBioMedicine ; 43: 620-631, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-31076346

RESUMO

BACKGROUND: Bone destruction is one of many severe complications that occurs in patients with rheumatoid arthritis (RA) and current therapies are unable to cure this manifestation. This study here aims to determine whether GMSC can directly inhibit osteoclast formation and eventually attenuate osteoclastogenesis and bone erosion in an inflammatory milieu. METHOD: GMSC were co-cultured with osteoclast precursors with or without CD39 inhibitor, CD73 inhibitor or adenosine receptors inhibitors pretreatment and osteoclast formation were evaluated in vitro. 2×10^6 GMSC per mouse were transferred to CIA mice and pathology scores, the frequency of osteoclasts, bone erosion in joints were assessed in vivo. FINDING: GMSC but not control cells, markedly suppressed human or mice osteoclastogenesis in vitro. GMSC treatment also resulted in a dramatically decreased level of NF-κB p65/p50 in osteoclasts in vitro. Infusion of GMSC to CIA significantly attenuated the severity of arthritis, pathology scores, frequency of osteoclasts, particularly bone erosion, as well as a decreased expression of RANKL in synovial tissues in vivo. Blockade of CD39/CD73 or adenosine receptors has significantly abrogated the suppressive ability of GMSC in vitro and therapeutic effect of GMSC on bone erosion during CIA in vivo. INTERPRETATION: GMSC inhibit osteoclast formation in vitro and in vivo partially via CD39-CD73-adenosine signals. Manipulation of GMSC may have a therapeutic implication on rheumatoid arthritis and other bone erosion related diseases. FUND: This study was supported by grants from the National Key R&D Program of China (2017YFA0105801 to F.H); the Zhujiang Innovative and Entrepreneurial Talent Team Award of Guangdong Province (2016 ZT 06S 252 to F·H) and National Institutes of Health (R01 AR059103, R61 AR073409 and NIH Star Award to S.G.Z).


Assuntos
Adenosina/metabolismo , Antígenos CD/metabolismo , Apirase/metabolismo , Gengiva/citologia , Células-Tronco Mesenquimais/citologia , Células-Tronco Mesenquimais/metabolismo , Osteogênese , Transdução de Sinais , Animais , Artrite Experimental , Artrite Reumatoide/diagnóstico por imagem , Artrite Reumatoide/etiologia , Artrite Reumatoide/metabolismo , Artrite Reumatoide/patologia , Doenças Autoimunes/diagnóstico por imagem , Doenças Autoimunes/etiologia , Doenças Autoimunes/metabolismo , Doenças Autoimunes/patologia , Biomarcadores , Linhagem Celular , Feminino , Fibroblastos/metabolismo , Humanos , Camundongos , Osteoclastos/metabolismo , Tomografia Computadorizada por Raios X
16.
Orv Hetil ; 160(17): 646-653, 2019 Apr.
Artigo em Húngaro | MEDLINE | ID: mdl-31010308

RESUMO

High salt intake, which is common in the Western world, is the cause of several lifestyle diseases. Recent investigations shed light on novel extrarenal processes, which play role in the maintenance of sodium balance. In the short term, sodium storage of the skin may serve as a buffer against volume overload arising from the osmotic properties of sodium. Increased tissue sodium concentration may also potentiate immune response against infections. In the long run, however, tissue sodium concentration over a certain limit may initiate pathophysiological processes by provoking inflammatory response. Due to the immune modulating role of sodium, the effector cells of the innate as well as the adaptive immune system are activated, while certain regulator cells of the same systems are repressed, ultimately resulting in a proinflammatory state characterized by the imbalance of the immune system. Experiments applying dietary salt overload/salt depletion imply the role of sodium in the initiation/exacerbation of several diseases. Thus the relationship between sodium and the immune system may give an explanation to the pathomechanism of diseases with so far unknown origin such as hypertonia (primary, salt sensitive) or autoimmune diseases - all these putting tremendous pressure on the healthcare system due to their increasing incidence. Orv Hetil. 2019; 160(17): 646-653.


Assuntos
Doenças Autoimunes/etiologia , Sistema Imunitário , Imunomodulação , Macrófagos/imunologia , Cloreto de Sódio na Dieta/metabolismo , Sódio , Autoimunidade , Humanos , Cloreto de Sódio , Cloreto de Sódio na Dieta/efeitos adversos , Linfócitos T
17.
Allergol Int ; 68(3): 301-308, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31000444

RESUMO

The aim of this review was to provide an updated overview of drug-induced hypersensitivity syndrome (DiHS)/drug reaction with eosinophilia and systemic symptoms (DRESS). Several new insights have been made, particularly with regards to the diagnosis, pathogenesis and care of some important complications and sequelae. The indication of herpesvirus reactivations in diagnosis in the assessment of disease severity is now better specified. Nevertheless, because fatal complications and autoimmune sequelae have been under-recognized, there is a clear need to identify effective parameters for assessing disease severity and predicting prognosis of the disease in the early phase. In this regard, we have established a scoring system that can be used to monitor severity, predict prognosis and stratify the risk of developing severe complications including fatal cytomegalovirus (CMV) disease. Regulatory T cells are likely to be central to the mechanism and would represent potential targets for therapeutic approaches that can ameliorate inflammatory responses occurring at the acute phase while preventing the subsequent development of harmful outcomes, such as CMV disease and autoimmune diseases.


Assuntos
Síndrome de Hipersensibilidade a Medicamentos/diagnóstico , Síndrome de Hipersensibilidade a Medicamentos/patologia , Corticosteroides/uso terapêutico , Doenças Autoimunes/etiologia , Doenças Autoimunes/prevenção & controle , Síndrome de Hipersensibilidade a Medicamentos/complicações , Síndrome de Hipersensibilidade a Medicamentos/tratamento farmacológico , Herpesviridae/fisiologia , Humanos , Prognóstico , Índice de Gravidade de Doença , Linfócitos T Reguladores/fisiologia , Ativação Viral
18.
Autoimmun Rev ; 18(6): 607-614, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30959217

RESUMO

Autoimmune diseases (ADs) are a broad spectrum of disorders featured by the body's immune responses being directed against its own tissues, resulting in prolonged inflammation and subsequent tissue damage. Recently, the exposure to ambient air pollution has been implicated in the occurrence and development of ADs. Mechanisms linking air pollution exposures and ADs mainly include systemic inflammation, increased oxidative stress, epigenetic modifications induced by exposures and immune response caused by airway damage. The lung may be an autoimmunity initiation site in autoimmune diseases (ADs). Air pollutants can bind to the Aryl hydrocarbon receptor (AHR) to regulate Th17 and Treg cells. Oxidative stress and inducible bronchus associated lymphoid tissue caused by the pollutants can influence T, B cells, resulting in the production of proinflammatory cytokines. These cytokines stimulate B cell and dendritic cells, resulting in a lot of antibodies and self-reactive T lymphocytes. Moreover, air pollutants may induce epigenetic changes to contribute to ADs. In this review, we will concern the associations between air pollution and immune-inflammatory responses, as well as mechanisms linking air pollution exposure and autoimmunity. In addition, we focus on the potential roles of air pollution in major autoimmune diseases including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), multiple sclerosis (MS), and type 1 diabetes mellitus (T1DM).


Assuntos
Poluição do Ar/efeitos adversos , Doenças Autoimunes/etiologia , Doenças Autoimunes/imunologia , Humanos
19.
Am J Clin Dermatol ; 20(4): 539-564, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30997665

RESUMO

The autoinflammatory diseases comprise a broad spectrum of disorders characterized by unchecked activation of the innate immune system. Whereas aberrations in adaptive immunity have long been identified in 'autoimmune' disorders, the concept of 'autoinflammation' emerged relatively recently, first describing a group of clinical disorders characterized by spontaneous episodes of systemic inflammation without manifestations typical of autoimmune disorders. Improved knowledge of innate immune mechanisms, coupled with remarkable progress in genomics and an expanding number of clinical cases, has since led to an increasing number of disorders classified as autoinflammatory or containing an autoinflammatory component. Biologic therapies targeting specific components of the innate immune system have provided immense clinical benefit, and have further elucidated the role of innate immunity in autoinflammatory disorders. This article reviews the basic mechanisms of autoinflammation, followed by an update on the pathophysiology and treatment of the monogenic and multifactorial autoinflammatory diseases, and the common dermatologic conditions in which autoinflammation plays a major role.


Assuntos
Doenças Autoimunes/tratamento farmacológico , Fatores Biológicos/uso terapêutico , Doenças Hereditárias Autoinflamatórias/tratamento farmacológico , Inflamação/tratamento farmacológico , Doenças Autoimunes/etiologia , Fatores Biológicos/farmacologia , Doenças Hereditárias Autoinflamatórias/etiologia , Humanos , Imunidade Inata/efeitos dos fármacos , Inflamação/etiologia , Pele/efeitos dos fármacos , Pele/imunologia , Resultado do Tratamento
20.
Immunity ; 50(4): 907-923, 2019 04 16.
Artigo em Inglês | MEDLINE | ID: mdl-30995506

RESUMO

Type I interferons (IFNs) (IFN-α, IFN-ß) and type III IFNs (IFN-λ) share many properties, including induction by viral infection, activation of shared signaling pathways, and transcriptional programs. However, recent discoveries have revealed context-specific functional differences. Here, we provide a comprehensive review of type I and type III IFN activities, highlighting shared and distinct features from molecular mechanisms through physiological responses. Beyond discussing canonical antiviral functions, we consider the adaptive immune priming, anti-tumor, and autoimmune functions of IFNs. We discuss a model wherein type III IFNs serve as a front-line defense that controls infection at epithelial barriers while minimizing damaging inflammatory responses, reserving the more potent type I IFN response for when local responses are insufficient. In this context, we discuss current therapeutic applications targeting these cytokine pathways and highlight gaps in understanding of the biology of type I and type III IFNs in health and disease.


Assuntos
Interferon Tipo I/imunologia , Interferons/imunologia , Imunidade Adaptativa , Animais , Antivirais/uso terapêutico , Doenças Autoimunes/etiologia , Doenças Autoimunes/imunologia , Células Epiteliais/imunologia , Feminino , Humanos , Interferon Tipo I/efeitos adversos , Interferon Tipo I/uso terapêutico , Interferons/efeitos adversos , Interferons/uso terapêutico , Masculino , Troca Materno-Fetal/imunologia , Camundongos , Neoplasias/tratamento farmacológico , Neoplasias/imunologia , Especificidade de Órgãos , Gravidez , Transdução de Sinais/imunologia , Transcrição Genética , Transcriptoma , Viroses/tratamento farmacológico , Viroses/imunologia
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