Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 23.440
Filtrar
1.
Clin Rheumatol ; 39(11): 3223-3235, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32885345

RESUMO

Cytokine pathways and their signaling disorders can be the cause of onset and pathogenesis of many diseases such as autoimmune diseases and COVID-19 infection. Autoimmune patients may be at higher risk of developing infection due to the impaired immune responses, the use of immunosuppressive drugs, and damage to various organs. Increased secretion of inflammatory cytokines and intolerance of the patient's immune system to COVID-19 infection are the leading causes of hospitalization of these patients. The content used in this paper has been taken from English language articles (2005-2020) retrieved from the PubMed database and Google Scholar search engine using "COVID-19," "Autoimmune disease," "Therapeutic," "Pathogenesis," and "Pathway" keywords. The emergence of COVID-19 and its association with autoimmune disorders is a major challenge in the management of these diseases. The results showed that the use of corticosteroids in the treatment of autoimmune diseases can make diagnosis and treatment of COVID-19 more challenging by preventing the fever. Due to the common pathogenesis of COVID-19 and autoimmune diseases, the use of autoimmune drugs as a possible treatment option could help control the virus. KEY POINTS: • Inflammatory cytokines play an essential role in the pathogenesis of COVID-19 • ACE2 dysfunctions are related to the with COVID-19 and autoimmune diseases • The use autoimmune diseases drugs can be useful in treating COVID-19.


Assuntos
Artrite Reumatoide/imunologia , Infecções por Coronavirus/imunologia , Citocinas/imunologia , Diabetes Mellitus/imunologia , Lúpus Eritematoso Sistêmico/imunologia , Esclerose Múltipla/imunologia , Pneumonia Viral/imunologia , Artrite Reumatoide/tratamento farmacológico , Doenças Autoimunes/tratamento farmacológico , Doenças Autoimunes/imunologia , Betacoronavirus , Infecções por Coronavirus/tratamento farmacológico , Diabetes Mellitus/metabolismo , Humanos , Lúpus Eritematoso Sistêmico/tratamento farmacológico , Lúpus Eritematoso Sistêmico/metabolismo , Esclerose Múltipla/tratamento farmacológico , Pandemias , Peptidil Dipeptidase A/metabolismo , Pneumonia Viral/tratamento farmacológico
2.
Rheumatol Int ; 40(9): 1353-1360, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32654078

RESUMO

As of June 10th 2020 about 7.2 million individuals have tested positive for, and more than 410,000 have died due to COVID-19. In this review we outline the pathophysiology that underpins the potential use of anti-rheumatic therapies for severe COVID-19 infection and summarize the current evidence regarding the risk and outcome of COVID-19 in patients with systemic autoimmune diseases. Thus far there is no convincing evidence that any disease-modifying anti-rheumatic drug (conventional synthetic, biologic or targeted synthetic) including hydroxychloroquine, may protect against severe COVID-19 infection; answers about their possible usefulness in the management of the cytokine storm associated with severe COVID-9 infection will only arise from ongoing randomized controlled trials. Evidence on COVID-19 risk and outcome in patients with systemic autoimmune diseases is extremely limited; thus, any conclusions would be unsafe and should be seen with great caution. At present, the risk and severity (hospitalization, intensive care unit admission and death) of COVID-19 infection in people with autoimmune diseases do not appear particularly dissimilar to the general population, with the possible exception of hospitalization in patients exposed to high glucocorticoid doses. At this stage it is impossible to draw any conclusions for differences in COVID-19 risk and outcome between different autoimmune diseases and between the various immunomodulatory therapies used for them. More research in the field is obviously required, including as a minimum careful and systematic epidemiology and appropriately controlled clinical trials.


Assuntos
Antirreumáticos/uso terapêutico , Doenças Autoimunes/tratamento farmacológico , Infecções por Coronavirus/tratamento farmacológico , Síndrome da Liberação de Citocina/tratamento farmacológico , Pneumonia Viral/tratamento farmacológico , Anticorpos Monoclonais Humanizados/uso terapêutico , Doenças Autoimunes/epidemiologia , Doenças Autoimunes/imunologia , Betacoronavirus , Comorbidade , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/imunologia , Síndrome da Liberação de Citocina/imunologia , Humanos , Inibidores de Janus Quinases/uso terapêutico , Pandemias , Pneumonia Viral/epidemiologia , Pneumonia Viral/imunologia , Fatores de Risco , Índice de Gravidade de Doença , Inibidores do Fator de Necrose Tumoral/uso terapêutico
3.
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
4.
Scand J Immunol ; 92(4): e12945, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32697368

RESUMO

In the past decades, clinical and experimental evidence has demonstrated that psoriasis is an immune-mediated inflammatory disease of the skin that occurs in genetically susceptible individuals. Psoriasis also shows clear autoimmune pathomechanisms, but specific cellular targets for the onset and maintenance of psoriatic lesions were not established until 2014. Since then, four psoriasis autoantigens were discovered, namely cathelicidin LL-37, melanocytic ADAMTSL5, lipid antigen PLA2G4D and keratin 17. Autoreactive T cells against these autoantigens were found in a number of patients with moderate-to-severe plaque psoriasis. Moreover, the discovery of autoantibodies against LL-37 and ADAMTSL5 and their strong association with psoriatic arthritis (PsA) suggest a potential role of these autoantibodies in the pathogenesis of PsA. This review discusses the current studies on psoriatic autoantigens and the associated circulating autoantibodies and their mechanisms involved in the development and maintenance of psoriatic plaques. Recent autoimmune evidence fuelled the discussion on psoriasis as an autoimmune skin disorder and has the potential to develop new treatment strategies with protective and therapeutic antigen-targeted methods.


Assuntos
Autoanticorpos/imunologia , Autoantígenos/imunologia , Doenças Autoimunes/imunologia , Psoríase/imunologia , Proteínas ADAMTS/imunologia , Animais , Peptídeos Catiônicos Antimicrobianos/imunologia , Autoimunidade/imunologia , Fosfolipases A2 do Grupo IV/imunologia , Humanos , Queratina-17/imunologia
5.
Autoimmun Rev ; 19(9): 102617, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32663626

RESUMO

The role of the cytokines and receptors of the IL-1 family in inflammation is well known. Several cytokines of the family have a powerful inflammatory activity, with IL-1ß being the best-characterized factor. The inflammatory activity of IL-1 cytokines is regulated by other factors of the family, including receptor antagonists, soluble receptors and anti-inflammatory cytokines. The causative role of IL-1ß is well-established in autoinflammatory diseases, mainly due to gain-of-function mutations in genes encoding the IL-1ß-maturing inflammasome. Exaggerated production of IL-1ß and IL-18 correlates with disease and disease severity also in several autoimmune and chronic inflammatory and degenerative pathologies, although it is not clear whether they have a causative role or are only involved in the downstream disease symptoms. A better understanding of the pathological role of IL-1 family cytokines in autoimmunity involves a deeper evaluation, in the pathological situations, of the possible anomalies in the feed-back anti-inflammatory mechanisms that in physiological reactions control and dump IL-1-mediated inflammation. Thus, we expect that IL-1 cytokines may be pathogenic only when, in addition to enhanced production, there is a concomitant failure of their control mechanisms. In this review we will examine the current knowledge on the role of IL-1 family cytokines in autoimmune and chronic inflammatory and degenerative diseases, with a particular focus on their endogenous control mechanisms, mainly based on soluble receptors/inhibitors and receptor antagonists. This will allow us to formulate a knowledge-based hypothesis on the involvement of IL-1 cytokines in the pathogenesis vs. the clinical features of these diseases.


Assuntos
Doenças Autoimunes/imunologia , Interleucina-1/classificação , Interleucina-1/imunologia , Doenças Autoimunes/patologia , Autoimunidade , Humanos , Inflamassomos , Inflamação
6.
Nat Commun ; 11(1): 3761, 2020 07 28.
Artigo em Inglês | MEDLINE | ID: mdl-32724101

RESUMO

Chronic immune-mediated diseases of adulthood often originate in early childhood. To investigate genetic associations between neonatal immunity and disease, we map expression quantitative trait loci (eQTLs) in resting myeloid cells and CD4+ T cells from cord blood samples, as well as in response to lipopolysaccharide (LPS) or phytohemagglutinin (PHA) stimulation, respectively. Cis-eQTLs are largely specific to cell type or stimulation, and 31% and 52% of genes with cis-eQTLs have response eQTLs (reQTLs) in myeloid cells and T cells, respectively. We identified cis regulatory factors acting as mediators of trans effects. There is extensive colocalisation between condition-specific neonatal cis-eQTLs and variants associated with immune-mediated diseases, in particular CTSH had widespread colocalisation across diseases. Mendelian randomisation shows causal neonatal gene expression effects on disease risk for BTN3A2, HLA-C and others. Our study elucidates the genetics of gene expression in neonatal immune cells, and aetiological origins of autoimmune and allergic diseases.


Assuntos
Doenças Autoimunes/genética , Desenvolvimento Infantil/fisiologia , Regulação da Expressão Gênica no Desenvolvimento/imunologia , Hipersensibilidade/genética , Locos de Características Quantitativas/imunologia , Doenças Autoimunes/imunologia , Butirofilinas/genética , Butirofilinas/metabolismo , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD4-Positivos/metabolismo , Catepsina H/genética , Catepsina H/metabolismo , Criança , Pré-Escolar , Conjuntos de Dados como Assunto , Sangue Fetal/citologia , Perfilação da Expressão Gênica , Redes Reguladoras de Genes/imunologia , Predisposição Genética para Doença , Estudo de Associação Genômica Ampla , Antígenos HLA-C/genética , Antígenos HLA-C/metabolismo , Humanos , Hipersensibilidade/imunologia , Lactente , Recém-Nascido , Análise da Randomização Mendeliana , Células Mieloides/imunologia , Células Mieloides/metabolismo , Análise de Sequência com Séries de Oligonucleotídeos , Polimorfismo de Nucleotídeo Único , Estudos Prospectivos
11.
Adv Gerontol ; 33(2): 246-255, 2020.
Artigo em Russo | MEDLINE | ID: mdl-32593238

RESUMO

Aging is a very complex process, resulting in dysregulation of multiple systems. The most prominent changes in immunological function, termed «immunosenescence¼, are diminished immune response against infection, increased levels of pro-inflammatory mediators and increased risk of autoimmunity. Immunoscenescence is accompanied by the low-grade aseptic inflammation observed commonly in elderly people - «inflammaging¼, which is associated with a higher incidence of chronic non-infectious age-associated diseases. The article discusses the main changes in innate and adaptive immunity in aging and their impact on the induction of autoimmune processes, provides data on the frequency of autoantibody detection in the elderly and the clinical features of some autoimmune diseases debuting at this age.


Assuntos
Envelhecimento/imunologia , Doenças Autoimunes/imunologia , Autoimunidade , Imunossenescência/imunologia , Imunidade Adaptativa , Idoso , Humanos , Imunidade Inata , Inflamação
12.
J Infect Public Health ; 13(9): 1196-1201, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32534944

RESUMO

The aging-associated decline of biological functions represents an important contributor to the increase in morbidity and mortality of human beings. Of these biological functions deterioration; there is a significant decline in the heart function, impairments in the lungs gas exchange, and impairments in the immune function. Many alterations in the body humeral and cellular immune response were observed with ageing process: The circulating pro-inflammatory cytokines are increased, the naive lymphocytes are decreased, the numbers of the antigen-presenting cells areelevated and the overall response is impaired. In addition, ageing is associated with a progressive restriction in the telomere length. Telomeres are located at chromosomes ends and play an essential role in preserving chromosome stability. Also, telomere length is very important to the immune system, because of the high sensitivity of the immune cells to the shortening of telomeres. Telomeres shortening adversely affect the immune cells' function and developments. These adverse changes increased the susceptibility for severe infection, risk of hospitalization, and even death. Elderly COVID-19 patients are at a real risk of complications due to impaired immune function, cytokine storm and defective respiratory function. Administration of anti-ageing immunomodulation factors like Nicotinamide Adenine Dinucleotide NAD+ can minimize these changes through its potent immunomodulation and longevity effects. NAD+ has a direct inhibitory effect on PARP-1 and can prevent pro-inflammatory cytokines over-activation. Increasing the NAD+ level will also result in stabilizing telomeres and this has a positive impact on immune cells function.


Assuntos
Envelhecimento/imunologia , Infecções por Coronavirus/imunologia , NAD/imunologia , NAD/metabolismo , Pneumonia Viral/imunologia , Encurtamento do Telômero/imunologia , Doenças Autoimunes/imunologia , Betacoronavirus , Infecções por Coronavirus/tratamento farmacológico , Citocinas/imunologia , Humanos , NAD/uso terapêutico , Pandemias , Pneumonia Viral/tratamento farmacológico , Poli(ADP-Ribose) Polimerase-1/antagonistas & inibidores
14.
Medicine (Baltimore) ; 99(22): e20437, 2020 May 29.
Artigo em Inglês | MEDLINE | ID: mdl-32481446

RESUMO

To study the changes of pancreas, thyroid, adrenal, parathyroid and gonadal organ-specific antibodies in patients with type 1 diabetic patients and to explore the risk of development to other endocrine gland autoimmune diseases.Fifty one patients with type 1 diabetes mellitus were selected. ELISA was used to detect islet, adrenal gland, Parathyroid, gonadal organ-specific antibody levels, the level of thyroid-related antibodies by lectrochemiluminescence.Compared with the healthy control group, the levels of the 17-α-OHAb, 21-OHAb, NALP5Ab, P450sccAb, and CaSRAb in the T1DM group were significantly higher. GADAb-positive patients were more likely to have TPOAb-positive patients than GADAb-negative patients, and the positive rate of 2 thyroid antibodies in GADAb-positive patients was significantly higher than that in GADAb-negative patients. The presence of these antibodies is related to the age of onset of type 1 diabetes or Patient age. In combination with 1 or 2 islet antibody-positive patients, the combined non-islet antibody positive rate was higher than that of islet antibody-negative patients.Patients with type 1 diabetes with other autoimmune diseases at risk significantly increased compared with normal, of which the most common thyroid autoimmune disease, thyroid antibodies and hormone levels should be routinely detected at the first visit and long-term follow-up.


Assuntos
Doenças Autoimunes/epidemiologia , Doenças Autoimunes/imunologia , Diabetes Mellitus Tipo 1/epidemiologia , Diabetes Mellitus Tipo 1/imunologia , Adolescente , Adulto , Anticorpos/sangue , Doenças Autoimunes/sangue , Criança , Pré-Escolar , Diabetes Mellitus Tipo 1/sangue , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Adulto Jovem
16.
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
17.
Zhongguo Xue Xi Chong Bing Fang Zhi Za Zhi ; 32(2): 203-207, 2020 Apr 26.
Artigo em Chinês | MEDLINE | ID: mdl-32458614

RESUMO

Recently, the incidence of infectious diseases continues to decline in many developed countries; however, the incidence of autoimmune diseases and allergic asthma appears a tendency towards a rise over years. "Hygiene hypothesis" provides new insights into the treatment of autoimmune disorders and allergic diseases based on parasitic infections. Increasing evidence shows that parasitic infections may effectively inhibit the development of diabetes, multiple sclerosis, inflammatory bowel disease, rheumatoid arthritis and allergic asthma. There are complex mechanisms underlying the relationship between parasitic infections and "hygiene hypothesis", among which regulatory T (Treg) cells and Th17 cells are becoming a hot topic of research. This paper reviews the progresses in the research on the relationship between parasitic infections and "hygiene hypothesis", and summarizes the roles of Treg cells and Th17 cells in the interplay between parasitic infections and "hygiene hypothesis".


Assuntos
Hipótese da Higiene , Doenças Parasitárias , Doenças Autoimunes/imunologia , Doenças Autoimunes/parasitologia , Humanos , Higiene , Doenças Parasitárias/imunologia , Células Th17/imunologia
18.
Autoimmun Rev ; 19(6): 102532, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32234402

RESUMO

The human leukocytes antigen (HLA)-DRB1*16:02 allele has been suggested to be associated with many autoimmune diseases. However, a validation of the results of the different studies by a comprehensive analysis of the corresponding meta data is lacking. In this study, we performed a meta-analysis of the association between HLA-DRB1*16:02 allele with various autoimmune disorders. Our analysis shows that HLA-DRB1*16:02 allele was associated with systemic lupus erythematosus, anti-N-Methyl-d-Aspartate receptor (NMDAR) encephalitis, Graves' disease, myasthenia gravis, neuromyelitis optica and antibody-associated systemic vasculitis with microscopic polyangiitis (AASV-MPA). However, no such association was found for multiple sclerosis, autoimmune hepatitis type 1, rheumatoid arthritis, type 1 diabetes and Vogt-Koyanagi-Harada syndrome. Re-analysis of the studies after their categorization into autoantibody-dependent and T cell-dependent autoimmune diseases revealed that the HLA-DRB1*16:02 allele was strongly associated with disorder predominantly mediated by autoantibodies (OR = 1.93; 95% CI = 1.63-2.28, P = 1.95 × 10-14) but not with those predominantly mediated by T cells (OR = 1.08; 95% CI = 0.87-1.34, P = .474). In addition, amino acid sequence alignment of common HLA-DRB1 subtypes demonstrated that HLA-DRB1*16:02 carries a unique motif of amino acid residues at position 67-74 which encodes the third hypervariable region. Taken together, the distinct pattern of disease association and the unique amino acid sequence of the third hypervariable region of the HLA-DRB1 provide some hints on how HLA-DRB1*16:02 is involved in the pathogenesis of autoimmune diseases.


Assuntos
Alelos , Autoanticorpos/imunologia , Doenças Autoimunes/genética , Doenças Autoimunes/imunologia , Predisposição Genética para Doença , Cadeias HLA-DRB1/genética , Humanos
19.
Autoimmun Rev ; 19(6): 102534, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32234403

RESUMO

INTRODUCTION: The complement system, an essential part of the innate immune system, is involved in various autoimmune diseases. Activation of the complement system by autoantibodies results in immune activation and tissue damage. At the moment little is known about the role of the complement system in autoimmune liver disease, including primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) and autoimmune hepatitis (AIH). Since inhibition of the complement system is currently being tested in several autoimmune diseases as a therapeutic option, its role in autoimmune liver disease requires further clarification. METHODS: A review of the literature was performed on studies investigating complement activation in PBC, PSC and AIH. Since data on AIH were lacking immunohistochemical staining for IgG, C1q, C3d, C4d and C5b9 was performed on liver tissue of nine AIH patients, two healthy controls and one positive control (acute liver failure caused by paracetamol intoxication). RESULTS: Immunohistochemical analysis in AIH revealed increased production of C3 and C4 by hepatocytes. Despite a strong staining for IgG in the immune infiltrate in AIH, C3d, C4d and C5b9 deposition was only present in one AIH patient and the deposition was restricted to the interface between portal tracts and liver parenchyma. No deposition was found in all other AIH patients or healthy controls. Literature review showed raised plasma C3 and C4 levels in AIH, PBC and PSC patients compared to healthy controls. For PBC and PSC no complement depositions at the bile ducts were reported. CONCLUSION AND DISCUSSION: Although complement is involved in various autoimmune diseases, the role of complement in autoimmune liver disease seems limited. Therefore it is unlikely that complement inhibition will become a novel treatment option for these diseases.


Assuntos
Doenças Autoimunes/imunologia , Doenças Autoimunes/patologia , Ativação do Complemento , Hepatopatias/imunologia , Hepatopatias/patologia , Colangite Esclerosante/imunologia , Colangite Esclerosante/patologia , Hepatite Autoimune/imunologia , Hepatite Autoimune/patologia , Humanos , Cirrose Hepática Biliar/imunologia , Cirrose Hepática Biliar/patologia
20.
Autoimmun Rev ; 19(6): 102535, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32234407

RESUMO

Glaucoma is characterized by retinal ganglion cell (RGC) neurodegeneration. Elevated intraocular pressure (IOP) is a major risk factor however, mechanisms independent of IOP play a role in RGC pathology. Both antibodies and CD4 T-cells as well as microbiota take part in the pathogenesis of both glaucoma and rheumatoid arteritis (RA).Heat shock proteins (HSPs) which originate in bacteria cross-react with RCG epitopes and were involved in rat model of retinal injury. Enhanced expression of HSPs in the retina was associated with glaucoma-like neuropathology and previous studies have also suggested a pathogenic role for HSPs in RA. In view of these data we suggest that glaucoma should be included in the spectrum of autoimmune diseases and that proven medications for RA should be adopted as an innovative IOP -independent therapeutic strategy for glaucoma.


Assuntos
Doenças Autoimunes/imunologia , Doenças Autoimunes/patologia , Glaucoma/imunologia , Glaucoma/patologia , Animais , Modelos Animais de Doenças , Proteínas de Choque Térmico , Humanos , Pressão Intraocular , Células Ganglionares da Retina/patologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA