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[PMID]:29295985
[Au] Autor:Conrad C; Di Domizio J; Mylonas A; Belkhodja C; Demaria O; Navarini AA; Lapointe AK; French LE; Vernez M; Gilliet M
[Ad] Endereço:Department of Dermatology, University Hospital CHUV, Lausanne, 1011, Switzerland. curdin.conrad@chuv.ch.
[Ti] Título:TNF blockade induces a dysregulated type I interferon response without autoimmunity in paradoxical psoriasis.
[So] Source:Nat Commun;9(1):25, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Although anti-tumor necrosis factor (TNF) agents are highly effective in the treatment of psoriasis, 2-5% of treated patients develop psoriasis-like skin lesions called paradoxical psoriasis. The pathogenesis of this side effect and its distinction from classical psoriasis remain unknown. Here we show that skin lesions from patients with paradoxical psoriasis are characterized by a selective overexpression of type I interferons, dermal accumulation of plasmacytoid dendritic cells (pDC), and reduced T-cell numbers, when compared to classical psoriasis. Anti-TNF treatment prolongs type I interferon production by pDCs through inhibition of their maturation. The resulting type I interferon overexpression is responsible for the skin phenotype of paradoxical psoriasis, which, unlike classical psoriasis, is independent of T cells. These findings indicate that paradoxical psoriasis represents an ongoing overactive innate inflammatory process, driven by pDC-derived type I interferon that does not lead to T-cell autoimmunity.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Autoimunidade/imunologia
Interferon Tipo I/imunologia
Psoríase/imunologia
Fator de Necrose Tumoral alfa/imunologia
[Mh] Termos MeSH secundário: Adalimumab/efeitos adversos
Adalimumab/imunologia
Adalimumab/uso terapêutico
Adolescente
Adulto
Idoso
Animais
Anticorpos Monoclonais/efeitos adversos
Anticorpos Monoclonais/uso terapêutico
Autoimunidade/efeitos dos fármacos
Células Cultivadas
Doença de Crohn/tratamento farmacológico
Doença de Crohn/imunologia
Doença de Crohn/metabolismo
Citocinas/genética
Citocinas/imunologia
Citocinas/metabolismo
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/imunologia
Células Dendríticas/metabolismo
Feminino
Seres Humanos
Infliximab/efeitos adversos
Infliximab/imunologia
Infliximab/uso terapêutico
Interferon Tipo I/genética
Interferon Tipo I/metabolismo
Masculino
Camundongos Endogâmicos BALB C
Meia-Idade
Psoríase/induzido quimicamente
Linfócitos T/efeitos dos fármacos
Linfócitos T/imunologia
Linfócitos T/metabolismo
Fator de Necrose Tumoral alfa/antagonistas & inibidores
Fator de Necrose Tumoral alfa/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Cytokines); 0 (Interferon Type I); 0 (Tumor Necrosis Factor-alpha); B72HH48FLU (Infliximab); FYS6T7F842 (Adalimumab)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02466-4


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[PMID]:28455189
[Au] Autor:Kelly SH; Shores LS; Votaw NL; Collier JH
[Ad] Endereço:Duke University, Department of Biomedical Engineering, United States.
[Ti] Título:Biomaterial strategies for generating therapeutic immune responses.
[So] Source:Adv Drug Deliv Rev;114:3-18, 2017 May 15.
[Is] ISSN:1872-8294
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Biomaterials employed to raise therapeutic immune responses have become a complex and active field. Historically, vaccines have been developed primarily to fight infectious diseases, but recent years have seen the development of immunologically active biomaterials towards an expanding list of non-infectious diseases and conditions including inflammation, autoimmunity, wounds, cancer, and others. This review structures its discussion of these approaches around a progression from single-target strategies to those that engage increasingly complex and multifactorial immune responses. First, the targeting of specific individual cytokines is discussed, both in terms of delivering the cytokines or blocking agents, and in terms of active immunotherapies that raise neutralizing immune responses against such single cytokine targets. Next, non-biological complex drugs such as randomized polyamino acid copolymers are discussed in terms of their ability to raise multiple different therapeutic immune responses, particularly in the context of autoimmunity. Last, biologically derived matrices and materials are discussed in terms of their ability to raise complex immune responses in the context of tissue repair. Collectively, these examples reflect the tremendous diversity of existing approaches and the breadth of opportunities that remain for generating therapeutic immune responses using biomaterials.
[Mh] Termos MeSH primário: Autoimunidade/efeitos dos fármacos
Materiais Biocompatíveis/uso terapêutico
Citocinas/antagonistas & inibidores
Inflamação/tratamento farmacológico
Inflamação/imunologia
Vacinas/imunologia
[Mh] Termos MeSH secundário: Animais
Autoimunidade/imunologia
Citocinas/imunologia
Seres Humanos
Cicatrização/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Cytokines); 0 (Vaccines)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:28449370
[Au] Autor:Fozza C
[Ad] Endereço:Department of Clinical and Experimental Medicine, University of Sassari, Sassari, Italy.
[Ti] Título:The burden of autoimmunity in myelodysplastic syndromes.
[So] Source:Hematol Oncol;36(1):15-23, 2018 Feb.
[Is] ISSN:1099-1069
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The clinical history of patients with myelodysplastic syndromes (MDS) is characterised by bone marrow insufficiency as well as by the possible evolution into acute leukaemia. However a number of reports highlight the frequent occurrence of autoimmune manifestations involving different sites and organs. The present review will first describe the clinical pictures most often observed in MDS patients. The actual burden of autoimmunity will be then addressed by focusing on the few available registry studies. Finally, the potential collateral impact of specific treatments for MDS on the evolution of autoimmune disorders will be considered.
[Mh] Termos MeSH primário: Autoimunidade/imunologia
Síndromes Mielodisplásicas/complicações
[Mh] Termos MeSH secundário: Seres Humanos
Síndromes Mielodisplásicas/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1002/hon.2423


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[PMID]:28470667
[Au] Autor:Tanaka T; Zhang W; Sun Y; Shuai Z; Chida AS; Kenny TP; Yang GX; Sanz I; Ansari A; Bowlus CL; Ippolito GC; Coppel RL; Okazaki K; He XS; Leung PSC; Gershwin ME
[Ad] Endereço:Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, Davis, CA.
[Ti] Título:Autoreactive monoclonal antibodies from patients with primary biliary cholangitis recognize environmental xenobiotics.
[So] Source:Hepatology;66(3):885-895, 2017 09.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A major problem in autoimmunity has been identification of the earliest events that lead to breach of tolerance. Although there have been major advances in dissecting effector pathways and the multilineage immune responses to mitochondrial self-antigens in primary biliary cholangitis, the critical links between environmental factors and tolerance remain elusive. We hypothesized that environmental xenobiotic modification of the E2 subunit of the pyruvate dehydrogenase (PDC-E2) inner lipoyl domain can lead to loss of tolerance to genetically susceptible hosts. Previously we demonstrated that serum anti-PDC-E2 autoantibodies cross-react with the chemical xenobiotics 2-octynoic acid and 6,8-bis (acetylthio) octanoic acid and further that there is a high frequency of PDC-E2-specific peripheral plasmablasts. Herein we generated 104 recombinant monoclonal antibodies (mAbs) based on paired heavy-chain and light-chain variable regions of individual plasmablasts derived from primary biliary cholangitis patients. We identified 32 mAbs reactive with native PDC-E2, including 20 specific for PDC-E2 and 12 cross-reactive with both PDC-E2 and 2-octynoic acid and 6,8-bis (acetylthio) octanoic acid. A lower frequency of replacement somatic hypermutations, indicating a lower level of affinity maturation, was observed in the complementarity-determining regions of the cross-reactive mAbs in comparison to mAbs exclusively recognizing PDC-E2 or those for irrelevant antigens. In particular, when the highly mutated heavy-chain gene of a cross-reactive mAb was reverted to the germline sequence, the PDC-E2 reactivity was reduced dramatically, whereas the xenobiotic reactivity was retained. Importantly, cross-reactive mAbs also recognized lipoic acid, a mitochondrial fatty acid that is covalently bound to PDC-E2. CONCLUSION: Our data reflect that chemically modified lipoic acid or lipoic acid itself, through molecular mimicry, is the initial target that leads to the development of primary biliary cholangitis. (Hepatology 2017;66:885-895).
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Autoantígenos/imunologia
Autoimunidade/genética
Colangite/imunologia
Colangite/patologia
Xenobióticos/imunologia
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/metabolismo
Autoantígenos/genética
Autoimunidade/imunologia
Feminino
Amplificação de Genes
Seres Humanos
Immunoblotting
Masculino
Mimetismo Molecular/genética
Reação em Cadeia da Polimerase em Tempo Real
Sensibilidade e Especificidade
Ácido Tióctico/imunologia
Ácido Tióctico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Autoantigens); 0 (Xenobiotics); 73Y7P0K73Y (Thioctic Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/hep.29245


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[PMID]:27773684
[Au] Autor:Elkington P; Tebruegge M; Mansour S
[Ad] Endereço:NIHR Southampton Respiratory Biomedical Research Unit, Clinical and Experimental Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, UK. Electronic address: p.elkington@soton.ac.uk.
[Ti] Título:Tuberculosis: An Infection-Initiated Autoimmune Disease?
[So] Source:Trends Immunol;37(12):815-818, 2016 12.
[Is] ISSN:1471-4981
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tuberculosis (TB) is caused by Mycobacterium tuberculosis (Mtb) and provided original proof that an infectious agent can cause human disease. However, key steps in TB pathogenesis remain poorly understood. We propose that autoimmunity is a critical and overlooked process driving pathology in TB, and present clinical and experimental observations supporting this hypothesis.
[Mh] Termos MeSH primário: Doenças Autoimunes/imunologia
Mycobacterium tuberculosis/imunologia
Tuberculose/imunologia
[Mh] Termos MeSH secundário: Animais
Autoimunidade
Carga Bacteriana/imunologia
Seres Humanos
Hospedeiro Imunocomprometido
Controle de Infecções
Camundongos
Tuberculose/transmissão
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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[PMID]:29269694
[Au] Autor:Matsui T; Nakagawa K; Yamazaki K; Wada T; Kadoya M; Kaida K
[Ad] Endereço:Department of Neurology, Anti-aging and Vascular Medicine, National Defense Medical College.
[Ti] Título:[An anti-RNP antibody-positive case of aseptic meningitis induced by non-steroidal anti-inflammatory drugs in a young woman].
[So] Source:Rinsho Shinkeigaku;58(1):25-29, 2018 Jan 26.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:A 19-year-old woman developed high fever, headache, and nausea after taking Loxoprofen for pharyngitis, followed by disturbed consciousness and nuchal stiffness. The patient and her mother had a history of Raynaud's phenomenon. Cerebrospinal fluid (CSF) examination indicated a diagnosis of aseptic meningitis and revealed high levels of Q albumin and IgG index. Anti-RNP antibodies were positive in serum and CSF. Her symptoms disappeared immediately after cessation of Loxoprofen and a drug lymphocyte stimulation test was negative, confirming a diagnosis of non-steroidal anti-inflammatory drugs (NSAIDs)-induced aseptic meningitis. It should be kept in mind that an immune abnormality such as serum and CSF anti-RNP antibodies may play a role in development of NSAIDs-induced aseptic meningitis. A history of usage of NSAIDs and a thorough examination of collagen diseases are useful for identification of the origin of aseptic meningitis in a young woman.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/efeitos adversos
Anticorpos Antinucleares/sangue
Anticorpos Antinucleares/líquido cefalorraquidiano
Meningite Asséptica/diagnóstico
Meningite Asséptica/etiologia
Fenilpropionatos/efeitos adversos
Ribonucleoproteínas/imunologia
[Mh] Termos MeSH secundário: Acetaminofen/administração & dosagem
Adulto
Anti-Inflamatórios não Esteroides/administração & dosagem
Doenças Autoimunes/complicações
Doenças Autoimunes/diagnóstico
Autoimunidade
Biomarcadores/sangue
Biomarcadores/líquido cefalorraquidiano
Diagnóstico Diferencial
Substituição de Medicamentos
Feminino
Seres Humanos
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antibodies, Antinuclear); 0 (Biomarkers); 0 (Phenylpropionates); 0 (Ribonucleoproteins); 3583H0GZAP (loxoprofen); 362O9ITL9D (Acetaminophen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-001085


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[PMID]:28467828
[Au] Autor:Ooi JD; Petersen J; Tan YH; Huynh M; Willett ZJ; Ramarathinam SH; Eggenhuizen PJ; Loh KL; Watson KA; Gan PY; Alikhan MA; Dudek NL; Handel A; Hudson BG; Fugger L; Power DA; Holt SG; Coates PT; Gregersen JW; Purcell AW; Holdsworth SR; La Gruta NL; Reid HH; Rossjohn J; Kitching AR
[Ad] Endereço:Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria 3168, Australia.
[Ti] Título:Dominant protection from HLA-linked autoimmunity by antigen-specific regulatory T cells.
[So] Source:Nature;545(7653):243-247, 2017 05 11.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Susceptibility and protection against human autoimmune diseases, including type I diabetes, multiple sclerosis, and Goodpasture disease, is associated with particular human leukocyte antigen (HLA) alleles. However, the mechanisms underpinning such HLA-mediated effects on self-tolerance remain unclear. Here we investigate the molecular mechanism of Goodpasture disease, an HLA-linked autoimmune renal disorder characterized by an immunodominant CD4 T-cell self-epitope derived from the α3 chain of type IV collagen (α3 ). While HLA-DR15 confers a markedly increased disease risk, the protective HLA-DR1 allele is dominantly protective in trans with HLA-DR15 (ref. 2). We show that autoreactive α3 -specific T cells expand in patients with Goodpasture disease and, in α3 -immunized HLA-DR15 transgenic mice, α3 -specific T cells infiltrate the kidney and mice develop Goodpasture disease. HLA-DR15 and HLA-DR1 exhibit distinct peptide repertoires and binding preferences and present the α3 epitope in different binding registers. HLA-DR15-α3 tetramer T cells in HLA-DR15 transgenic mice exhibit a conventional T-cell phenotype (T ) that secretes pro-inflammatory cytokines. In contrast, HLA-DR1-α3 tetramer T cells in HLA-DR1 and HLA-DR15/DR1 transgenic mice are predominantly CD4 Foxp3 regulatory T cells (T cells) expressing tolerogenic cytokines. HLA-DR1-induced T cells confer resistance to disease in HLA-DR15/DR1 transgenic mice. HLA-DR15 and HLA-DR1 healthy human donors display altered α3 -specific T-cell antigen receptor usage, HLA-DR15-α3 tetramer Foxp3 T and HLA-DR1-α3 tetramer Foxp3 CD25 CD127 T dominant phenotypes. Moreover, patients with Goodpasture disease display a clonally expanded α3 -specific CD4 T-cell repertoire. Accordingly, we provide a mechanistic basis for the dominantly protective effect of HLA in autoimmune disease, whereby HLA polymorphism shapes the relative abundance of self-epitope specific T cells that leads to protection or causation of autoimmunity.
[Mh] Termos MeSH primário: Doença Antimembrana Basal Glomerular/imunologia
Autoimunidade/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Doença Antimembrana Basal Glomerular/patologia
Sequência de Bases
Linfócitos T CD4-Positivos/imunologia
Colágeno Tipo IV/química
Colágeno Tipo IV/imunologia
Citocinas/imunologia
Feminino
Fatores de Transcrição Forkhead/metabolismo
Subtipos Sorológicos de HLA-DR/imunologia
Antígeno HLA-DR1/imunologia
Seres Humanos
Epitopos Imunodominantes
Masculino
Camundongos
Camundongos Transgênicos
Modelos Moleculares
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Collagen Type IV); 0 (Cytokines); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (HLA-DR Serological Subtypes); 0 (HLA-DR1 Antigen); 0 (HLA-DR15 antigen); 0 (Immunodominant Epitopes)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1038/nature22329


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[PMID]:29315316
[Au] Autor:Dick J; Gan PY; Kitching AR; Holdsworth SR
[Ad] Endereço:Centre for Inflammatory Diseases, Monash University Department of Medicine, Clayton, Victoria, Australia.
[Ti] Título:The C3aR promotes macrophage infiltration and regulates ANCA production but does not affect glomerular injury in experimental anti-myeloperoxidase glomerulonephritis.
[So] Source:PLoS One;13(1):e0190655, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitides are autoimmune diseases associated with significant morbidity and mortality. They often affect the kidney causing rapidly progressive glomerulonephritis. While signalling by complement anaphylatoxin C5a though the C5a receptor is important in this disease, the role of the anaphylatoxin C3a signalling via the C3a receptor (C3aR) is not known. Using two different murine models of anti-myeloperoxidase (MPO) glomerulonephritis, one mediated by passive transfer of anti-MPO antibodies, the other by cell-mediated immunity, we found that the C3aR did not alter histological disease severity. However, it promoted macrophage recruitment to the inflamed glomerulus and inhibited the generation of MPO-ANCA whilst not influencing T cell autoimmunity. Thus, whilst the C3aR modulates some elements of disease pathogenesis, overall it is not critical in effector responses and glomerular injury caused by autoimmunity to MPO.
[Mh] Termos MeSH primário: Anticorpos Anticitoplasma de Neutrófilos/imunologia
Complemento C3a/metabolismo
Glomerulonefrite/patologia
Macrófagos/patologia
Peroxidase/imunologia
Receptores de Complemento/fisiologia
[Mh] Termos MeSH secundário: Animais
Formação de Anticorpos
Autoimunidade
Glomerulonefrite/imunologia
Imunidade Celular
Camundongos
Camundongos Endogâmicos C57BL
Receptores de Complemento/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Antineutrophil Cytoplasmic); 0 (Receptors, Complement); 80295-42-7 (Complement C3a); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190655


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[PMID]:29221598
[Au] Autor:Schett G
[Ad] Endereço:Department of Internal Medicine 3 and Institute for Clinical Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum, Erlangen, Germany. Electronic address: georg.schett@uk-erlangen.de.
[Ti] Título:The role of ACPAs in at-risk individuals: Early targeting of the bone and joints.
[So] Source:Best Pract Res Clin Rheumatol;31(1):53-58, 2017 02.
[Is] ISSN:1532-1770
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Autoimmunity precedes inflammation in patients with rheumatoid arthritis (RA), opening the possibility to search for early changes in the tissue preceding the onset of systemic inflammation. Autoantibodies are important and early drivers of bone damage in RA. This article summarizes current evidence for the role of RA-related autoantibodies in mediating bone loss. Rheumatoid factor (RF) and antibodies recognizing modified (citrullinated) proteins have been used as diagnostic markers for RA over many years. Their role as pathogenic players, however, has long been unrecognized. Recently, several pieces of evidence suggested that bone-resorbing osteoclasts are highly responsive to RA-related autoantibodies, providing a novel association between autoimmunity and bone. These developments have allowed the unraveling of the underlying mechanisms, which are responsible for the well-known clinical observation that anti-citrullinated protein antibodies and RF are associated with a more severe disease course. Furthermore, these mechanisms also explain the onset of inflammation in the joints of RA patients.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Autoanticorpos/imunologia
Autoimunidade/imunologia
[Mh] Termos MeSH secundário: Osso e Ossos/imunologia
Seres Humanos
Peptídeos Cíclicos/imunologia
Fator Reumatoide/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Peptides, Cyclic); 9009-79-4 (Rheumatoid Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE


  10 / 14683 MEDLINE  
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[PMID]:29221596
[Au] Autor:Joshua V; Chatzidionisyou K; Catrina AI
[Ad] Endereço:Rheumatology Unit, Department of Medicine at Solna, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
[Ti] Título:Role of the lung in individuals at risk of rheumatoid arthritis.
[So] Source:Best Pract Res Clin Rheumatol;31(1):31-41, 2017 02.
[Is] ISSN:1532-1770
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Antibody-positive (seropositive) rheumatoid arthritis (RA) is a complex multiphasic disease developing in genetically susceptible individuals following environmental challenges (such as smoking). RA-associated autoantibodies can develop several years before any clinical signs of joint inflammation, suggesting that triggering of this autoimmunity occurs outside the joints. Epidemiological, clinical, and molecular studies in seropositive individuals at risk for developing RA as well as in early untreated RA suggest a potential role for mucosal sites (especially lung mucosa) as RA-associated autoimmunity trigger sites. This chapter summarizes clinical and molecular studies supporting the lung as a central site for autoimmunity initiation in RA.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Autoimunidade/imunologia
Pulmão/imunologia
[Mh] Termos MeSH secundário: Autoanticorpos/imunologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantibodies)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE



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