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[PMID]:29295972
[Au] Autor:Jabs F; Plum M; Laursen NS; Jensen RK; Mølgaard B; Miehe M; Mandolesi M; Rauber MM; Pfützner W; Jakob T; Möbs C; Andersen GR; Spillner E
[Ad] Endereço:Immunological Engineering, Department of Engineering, Aarhus University, 8000, Aarhus, Denmark.
[Ti] Título:Trapping IgE in a closed conformation by mimicking CD23 binding prevents and disrupts FcεRI interaction.
[So] Source:Nat Commun;9(1):7, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Anti-IgE therapeutics interfere with the ability of IgE to bind to its receptors on effector cells. Here we report the crystal structure of an anti-IgE single-domain antibody in complex with an IgE Fc fragment, revealing how the antibody inhibits interactions between IgE and the two receptors FcεRI and CD23. The epitope overlaps only slightly with the FcεRI-binding site but significantly with the CD23-binding site. Solution scattering studies of the IgE Fc reveal that antibody binding induces a half-bent conformation in between the well-known bent and extended IgE Fc conformations. The antibody acts as functional homolog of CD23 and induces a closed conformation of IgE Fc incompatible with FcεRI binding. Notably the antibody displaces IgE from both CD23 and FcεRI, and abrogates allergen-mediated basophil activation and facilitated allergen binding. The inhibitory mechanism might facilitate strategies for the future development of anti-IgE therapeutics for treatment of allergic diseases.
[Mh] Termos MeSH primário: Epitopos/química
Imunoglobulina E/química
Receptores de IgE/química
[Mh] Termos MeSH secundário: Anticorpos Anti-Idiotípicos/química
Anticorpos Anti-Idiotípicos/metabolismo
Sítios de Ligação
Cristalografia por Raios X
Epitopos/metabolismo
Seres Humanos
Imunoglobulina E/metabolismo
Fragmentos Fc das Imunoglobulinas/química
Fragmentos Fc das Imunoglobulinas/metabolismo
Modelos Moleculares
Ligação Proteica
Conformação Proteica
Receptores de IgE/metabolismo
Anticorpos de Domínio Único/química
Anticorpos de Domínio Único/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Anti-Idiotypic); 0 (Epitopes); 0 (Immunoglobulin Fc Fragments); 0 (Receptors, IgE); 0 (Single-Domain Antibodies); 0 (anti-IgE antibodies); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02312-7


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[PMID]:29192831
[Au] Autor:Johnson JR; Harker JA
[Ad] Endereço:1 School of Life and Health Sciences Aston University Birmingham, United Kingdom and.
[Ti] Título:Allergic Airway Disease: More than Meets the IgE?
[So] Source:Am J Respir Cell Mol Biol;57(6):631-632, 2017 12.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Alérgenos/imunologia
Asma/imunologia
Imunoglobulina E/imunologia
Pyroglyphidae/imunologia
Receptores de IgE/imunologia
[Mh] Termos MeSH secundário: Animais
Asma/patologia
Seres Humanos
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (Allergens); 0 (FCER1A protein, human); 0 (Receptors, IgE); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0271ED


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[PMID]:28886017
[Au] Autor:Moura RA; Quaresma C; Vieira AR; Gonçalves MJ; Polido-Pereira J; Romão VC; Martins N; Canhão H; Fonseca JE
[Ad] Endereço:Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal.
[Ti] Título:B-cell phenotype and IgD-CD27- memory B cells are affected by TNF-inhibitors and tocilizumab treatment in rheumatoid arthritis.
[So] Source:PLoS One;12(9):e0182927, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The use of TNF-inhibitors and/or the IL-6 receptor antagonist, tocilizumab, in rheumatoid arthritis (RA) have pleiotropic effects that also involve circulating B-cells. The main goal of this study was to assess the effect of TNF-inhibitors and tocilizumab on B-cell phenotype and gene expression in RA. METHODS: Blood samples were collected from untreated early RA (ERA) patients, established RA patients under methotrexate treatment, established RA patients before and after treatment with TNF-inhibitors and tocilizumab, and healthy donors. B-cell subpopulations were characterized by flow cytometry and B-cell gene expression was analyzed by real-time PCR on isolated B-cells. Serum levels of BAFF, CXCL13 and sCD23 were determined by ELISA. RESULTS: The frequency of total CD19+ B cells in circulation was similar between controls and all RA groups, irrespective of treatment, but double negative (DN) IgD-CD27- memory B cells were significantly increased in ERA and established RA when compared to controls. Treatment with TNF-inhibitors and tocilizumab restored the frequency of IgD-CD27- B-cells to normal levels, but did not affect other B cell subpopulations. TACI, CD95, CD5, HLA-DR and TLR9 expression on B-cells significantly increased after treatment with either TNF-inhibitors and/ or tocilizumab, but no significant changes were observed in BAFF-R, BCMA, CD69, CD86, CXCR5, CD23, CD38 and IgM expression on B-cells when comparing baseline with post-treatment follow-ups. Alterations in B-cell gene expression of BAFF-R, TACI, TLR9, FcγRIIB, BCL-2, BLIMP-1 and ß2M were found in ERA and established RA patients, but no significant differences were observed after TNF-inhibitors and tocilizumab treatment when comparing baseline and follow-ups. Serum levels of CXCL13, sCD23 and BAFF were not significantly affected by treatment with TNF-inhibitors and tocilizumab. CONCLUSIONS: In RA patients, the use of TNF-inhibitors and/ or tocilizumab treatment affects B-cell phenotype and IgD-CD27- memory B cells in circulation, but not B-cell gene expression levels.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Artrite Reumatoide/tratamento farmacológico
Artrite Reumatoide/imunologia
Subpopulações de Linfócitos B/imunologia
Memória Imunológica
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Anticorpos Monoclonais Humanizados/farmacologia
Artrite Reumatoide/diagnóstico
Artrite Reumatoide/metabolismo
Subpopulações de Linfócitos B/efeitos dos fármacos
Subpopulações de Linfócitos B/metabolismo
Biomarcadores
Quimiocina CXCL13/sangue
Seguimentos
Perfilação da Expressão Gênica
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Imunoglobulina D/metabolismo
Imunofenotipagem
Contagem de Linfócitos
Metotrexato/farmacologia
Metotrexato/uso terapêutico
Fenótipo
Receptores CXCR5/metabolismo
Receptores de IgE/sangue
Resultado do Tratamento
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Biomarkers); 0 (Chemokine CXCL13); 0 (Immunoglobulin D); 0 (Receptors, CXCR5); 0 (Receptors, IgE); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (Tumor Necrosis Factor-alpha); I031V2H011 (tocilizumab); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182927


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[PMID]:28832948
[Au] Autor:Köhnke T; Wittmann VK; Bücklein VL; Lichtenegger F; Pasalic Z; Hiddemann W; Spiekermann K; Subklewe M
[Ad] Endereço:Department of Medicine III, University Hospital, LMU Munich, Munich, Germany.
[Ti] Título:Diagnosis of CLL revisited: increased specificity by a modified five-marker scoring system including CD200.
[So] Source:Br J Haematol;179(3):480-487, 2017 Nov.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The modified Matutes score has been the basis for the diagnosis of chronic lymphocytic leukaemia (CLL) by flow cytometry for the past 15 years. To increase the specificity of the current score we systematically evaluated the diagnostic value of established as well as novel markers, such as CD200, in a large cohort of patients with untreated B-cell malignancies (n = 370). Double positivity for CD5 and CD23 was of very high value to differentiate between CLL and non-CLL cases. In addition, lack of FMC7 expression as well as CD79b expression intensity showed high sensitivity (90·4% and 92·3%) with acceptable specificity (74·4% and 76·9%). For surface IgM, low or absent expression displayed poor specificity in distinguishing CLL from non-CLL cases (51,3%; sensitivity 83,7%). Finally, CD200 positivity showed high sensitivity and specificity. Therefore, CD5/CD23, FMC7, CD79b and CD200 were included in our new CLLflow score, which retained high sensitivity (97·1% vs. 98·6% for the Matutes score, P = 0·38), but showed markedly increased specificity (87·2% vs. 53·8%, P < 0·001). These results were confirmed in our validation cohort (sensitivity 97·0% vs. 100%, P = not applicable; specificity 86·4% vs. 59·1%, P = 0·03). Our data support the use of our new CLLflow score for the diagnosis of CLL with significantly higher specificity.
[Mh] Termos MeSH primário: Antígenos CD/sangue
Biomarcadores Tumorais/sangue
Leucemia Linfocítica Crônica de Células B/diagnóstico
[Mh] Termos MeSH secundário: Antígenos CD5/sangue
Antígenos CD79/sangue
Diagnóstico Diferencial
Glicoproteínas/sangue
Seres Humanos
Imunoglobulina M/sangue
Imunofenotipagem
Receptores de IgE/sangue
Sensibilidade e Especificidade
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Biomarkers, Tumor); 0 (CD5 Antigens); 0 (CD79 Antigens); 0 (CD79B protein, human); 0 (FMC7 protein, human); 0 (Glycoproteins); 0 (Immunoglobulin M); 0 (Receptors, IgE); 0 (antigens, CD200)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14901


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[PMID]:28652400
[Au] Autor:Schroeder JT; Bieneman AP
[Ad] Endereço:Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, MD 21224 schray@jhmi.edu.
[Ti] Título:Activation of Human Basophils by A549 Lung Epithelial Cells Reveals a Novel IgE-Dependent Response Independent of Allergen.
[So] Source:J Immunol;199(3):855-865, 2017 Aug 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Evidence for epithelial cell (EC)-derived cytokines (e.g., thymic stromal lymphopoietin [TSLP]) activating human basophils remains controversial. We therefore hypothesize that ECs can directly activate basophils via cell-to-cell interaction. Basophils in medium alone or with IL-3 ± anti-IgE were coincubated with TSLP, IL-33, or IL-25. Analogous experiments cocultured basophils (1-72 h) directly with EC lines. Supernatants were tested for mediators and cytokines. Abs targeting receptors were tested for neutralizing effects. Lactic acid (pH 3.9) treatment combined with passive sensitization tested the role of IgE. Overall, IL-33 augmented IL-13 secretion from basophils cotreated with IL-3, with minimal effects on histamine and IL-4. Conversely, basophils (but not mast cells) released histamine and marked levels of IL-4/IL-13 (10-fold) when cocultured with A549 EC and IL-3, without exogenous allergen or IgE cross-linking stimuli. The inability to detect IL-33 or TSLP, or to neutralize their activity, suggested a unique mode of basophil activation by A549 EC. Half-maximal rates for histamine (4 h) and IL-4 (5 h) secretion were slower than observed with standard IgE-dependent activation. Ig stripping combined with passive sensitization ± omalizumab showed a dependency for basophil-bound IgE, substantiated by a requirement for cell-to-cell contact, aggregation, and FcεRI-dependent signaling. A yet unidentified IgE-binding lectin associated with A549 EC is implicated after discovering that LacNAc suppressed basophil activation in cocultures. These findings point to a lectin-dependent activation of basophil requiring IgE but independent of allergen or secreted cytokine. Pending further investigation, we predict this unique mode of activation is linked to inflammatory conditions whereby IgE-dependent activation of basophils occurs despite the absence of any known allergen.
[Mh] Termos MeSH primário: Alérgenos/imunologia
Basófilos/imunologia
Células Epiteliais/imunologia
Imunoglobulina E/imunologia
[Mh] Termos MeSH secundário: Células A549
Anticorpos Anti-Idiotípicos/farmacologia
Basófilos/efeitos dos fármacos
Basófilos/metabolismo
Comunicação Celular
Técnicas de Cocultura
Citocinas/farmacologia
Citocinas/secreção
Células Epiteliais/metabolismo
Liberação de Histamina
Seres Humanos
Imunoglobulina E/metabolismo
Interleucina-13/imunologia
Interleucina-13/secreção
Interleucina-17/farmacologia
Interleucina-3/imunologia
Interleucina-3/farmacologia
Interleucina-33/farmacologia
Interleucina-4/imunologia
Interleucina-4/secreção
Ácido Láctico/farmacologia
Lectinas/metabolismo
Mastócitos/metabolismo
Omalizumab/farmacologia
Receptores de IgE/imunologia
Receptores de IgE/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (Antibodies, Anti-Idiotypic); 0 (Cytokines); 0 (FcepsilonRI alpha-chain, human); 0 (IL25 protein, human); 0 (IL3 protein, human); 0 (IL33 protein, human); 0 (Interleukin-13); 0 (Interleukin-17); 0 (Interleukin-3); 0 (Interleukin-33); 0 (Lectins); 0 (Receptors, IgE); 0 (anti-IgE antibodies); 0 (interleukin-13, human); 0 (thymic stromal lymphopoietin); 207137-56-2 (Interleukin-4); 2P471X1Z11 (Omalizumab); 33X04XA5AT (Lactic Acid); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700055


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[PMID]:28637902
[Au] Autor:Ndaw VS; Abebayehu D; Spence AJ; Paez PA; Kolawole EM; Taruselli MT; Caslin HL; Chumanevich AP; Paranjape A; Baker B; Barnstein BO; Haque TT; Kiwanuka KN; Oskeritzian CA; Ryan JJ
[Ad] Endereço:Department of Biology, Virginia Commonwealth University, Richmond, VA 23284.
[Ti] Título:TGF-ß1 Suppresses IL-33-Induced Mast Cell Function.
[So] Source:J Immunol;199(3):866-873, 2017 Aug 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TGF-ß1 is involved in many pathological conditions, including autoimmune disorders, cancer, and cardiovascular and allergic diseases. We have previously found that TGF-ß1 can suppress IgE-mediated mast cell activation of human and mouse mast cells. IL-33 is a member of the IL-1 family capable of inducing mast cell responses and enhancing IgE-mediated activation. In this study, we investigated the effects of TGF-ß on IL-33-mediated mast cell activation. Bone marrow-derived mast cells cultured in TGF-ß1, ß2, or ß3 showed reduced IL-33-mediated production of TNF, IL-6, IL-13, and MCP-1 in a concentration-dependent manner. TGF-ß1 inhibited IL-33-mediated Akt and ERK phosphorylation as well as NF-κB- and AP-1-mediated transcription. These effects were functionally important, as TGF-ß1 injection suppressed IL-33-induced systemic cytokines in vivo and inhibited IL-33-mediated cytokine release from human mast cells. TGF-ß1 also suppressed the combined effects of IL-33 and IgE-mediated activation on mouse and human mast cells. The role of IL-33 in the pathogenesis of allergic diseases is incompletely understood. These findings, consistent with our previously reported effects of TGF-ß1 on IgE-mediated activation, demonstrate that TGF-ß1 can provide broad inhibitory signals to activated mast cells.
[Mh] Termos MeSH primário: Interleucina-33/imunologia
Mastócitos/imunologia
Fator de Crescimento Transformador beta1/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Citocinas/antagonistas & inibidores
Citocinas/biossíntese
Citocinas/imunologia
Seres Humanos
Imunoglobulina E/imunologia
Interleucina-6/biossíntese
Interleucina-6/imunologia
Ativação Linfocitária/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Mastócitos/efeitos dos fármacos
Mastócitos/metabolismo
Camundongos
NF-kappa B/genética
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores de IgE/imunologia
Fator de Transcrição AP-1/genética
Fator de Crescimento Transformador beta1/farmacologia
Fator de Crescimento Transformador beta3/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (IL33 protein, human); 0 (Interleukin-33); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Receptors, IgE); 0 (Transcription Factor AP-1); 0 (Transforming Growth Factor beta1); 0 (Transforming Growth Factor beta3); 37341-29-0 (Immunoglobulin E); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601983


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[PMID]:28629733
[Au] Autor:Yin Y; Bai Y; Olivera A; Desai A; Metcalfe DD
[Ad] Endereço:Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases,National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: yiny@niaid.nih.gov.
[Ti] Título:An optimized protocol for the generation and functional analysis of human mast cells from CD34 enriched cell populations.
[So] Source:J Immunol Methods;448:105-111, 2017 Sep.
[Is] ISSN:1872-7905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The culture of mast cells from human tissues such a cord blood, peripheral blood or bone marrow aspirates has advanced our understanding of human mast cells (huMC) degranulation, mediator production and response to pharmacologic agents. However, existing methods for huMC culture tend to be laborious and expensive. Combining technical approaches from several of these protocols, we designed a simplified and more cost effective approach to the culture of mast cells from human cell populations including peripheral blood and cryopreserved cells from lymphocytapheresis. On average, we reduced by 30-50 fold the amount of culture media compared to our previously reported method, while the total MC number generated by this method (2.46±0.63×10 vs. 2.4±0.28×10 , respectively, from 1.0×10 lymphocytapheresis or peripheral blood mononuclear blood cells [PBMCs]) was similar to our previous method (2.36±0.70×10 ), resulting in significant budgetary savings. In addition, we compared the yield of huMCs with or without IL-3 added to early cultures in the presence of stem cell factor (SCF) and interlukin-6 (IL-6) and found that the total MC number generated, while higher with IL-3 in the culture, did not reach statistical significance, suggesting that IL-3, often recommended in the culture of huMCs, is not absolutely required. We then performed a functional analysis by flow cytometry using standard methods and which maximized the data we could obtain from cultured cells. We believe these approaches will allow more laboratories to culture and examine huMC behavior going forward.
[Mh] Termos MeSH primário: Antígenos CD34/metabolismo
Separação Celular/métodos
Leucaférese
Mastócitos/metabolismo
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Antígenos CD34/imunologia
Biomarcadores/metabolismo
Orçamentos
Degranulação Celular
Diferenciação Celular
Linhagem da Célula
Proliferação Celular
Separação Celular/economia
Forma Celular
Células Cultivadas
Redução de Custos
Análise Custo-Benefício
Criopreservação
Meios de Cultura/metabolismo
Citometria de Fluxo
Seres Humanos
Interleucina-3/farmacologia
Interleucina-6/farmacologia
Leucaférese/economia
Mastócitos/efeitos dos fármacos
Mastócitos/imunologia
Fenótipo
Proteínas Proto-Oncogênicas c-kit/metabolismo
Receptores de IgE/metabolismo
Fator de Células-Tronco/farmacologia
Células-Tronco/efeitos dos fármacos
Células-Tronco/imunologia
Fatores de Tempo
Fluxo de Trabalho
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Biomarkers); 0 (Culture Media); 0 (IL3 protein, human); 0 (IL6 protein, human); 0 (Interleukin-3); 0 (Interleukin-6); 0 (Receptors, IgE); 0 (Stem Cell Factor); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE


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[PMID]:28554574
[Au] Autor:Zhang L; Yang C; Lewis JS; El-Mofty SK; Chernock RD
[Ad] Endereço:Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO 63110, USA.
[Ti] Título:p16 expression in follicular dendritic cell sarcoma: a potential mimicker of human papillomavirus-related oropharyngeal squamous cell carcinoma.
[So] Source:Hum Pathol;66:40-47, 2017 Aug.
[Is] ISSN:1532-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Follicular dendritic cell sarcoma is a rare mesenchymal neoplasm that most commonly occurs in cervical lymph nodes. It has histologic and clinical overlap with the much more common p16-positive human papillomavirus (HPV)-related squamous cell carcinoma of the oropharynx, which characteristically has nonkeratinizing morphology and often presents as an isolated neck mass. Not surprisingly, follicular dendritic cell sarcomas are commonly misdiagnosed as squamous cell carcinoma. Immunohistochemistry is helpful in separating the 2 entities. Follicular dendritic cell sarcoma expresses dendritic markers such as CD21 and CD23 and is almost always cytokeratin negative. However, in many cases of HPV-related oropharyngeal carcinoma, only p16 immunohistochemistry as a prognostic and surrogate marker for HPV is performed. p16 expression in follicular dendritic cell sarcoma has not been characterized. Here, we investigate the expression of p16 in follicular dendritic cell sarcoma and correlate it with retinoblastoma protein expression. A pilot study of dendritic marker expression in HPV-related oropharyngeal squamous cell carcinoma was also performed. We found that 4 of 8 sarcomas expressed p16 with strong and diffuse staining in 2 cases. In 2 of the 4 cases, p16 expression corresponded to loss of retinoblastoma protein expression. Dendritic marker expression (CD21 and CD23) was not found in HPV-related oropharyngeal squamous cell carcinomas. As such, positive p16 immunohistochemistry cannot be used as supportive evidence for the diagnosis of squamous cell carcinoma as strong and diffuse p16 expression may also occur in follicular dendritic cell sarcoma. Cytokeratins and dendritic markers are critical in separating the two tumor types.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Carcinoma de Células Escamosas/química
Inibidor p16 de Quinase Dependente de Ciclina/análise
Sarcoma de Células Dendríticas Foliculares/metabolismo
Neoplasias de Cabeça e Pescoço/química
Neoplasias Orofaríngeas/química
Infecções por Papillomavirus/metabolismo
[Mh] Termos MeSH secundário: Adulto
Carcinoma de Células Escamosas/patologia
Carcinoma de Células Escamosas/virologia
Sarcoma de Células Dendríticas Foliculares/patologia
Diagnóstico Diferencial
Feminino
Neoplasias de Cabeça e Pescoço/patologia
Neoplasias de Cabeça e Pescoço/virologia
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Missouri
Neoplasias Orofaríngeas/patologia
Neoplasias Orofaríngeas/virologia
Infecções por Papillomavirus/patologia
Infecções por Papillomavirus/virologia
Projetos Piloto
Valor Preditivo dos Testes
Receptores de Complemento 3d/análise
Receptores de IgE/análise
Proteína do Retinoblastoma/análise
Tennessee
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Cyclin-Dependent Kinase Inhibitor p16); 0 (P16 protein, human); 0 (Receptors, Complement 3d); 0 (Receptors, IgE); 0 (Retinoblastoma Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE


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[PMID]:28510589
[Au] Autor:Qu XL; Hei Y; Kang L; Yang XJ; Wang Y; Lu XZ; Xiao LH; Yang G
[Ad] Endereço:Ophthalmology Department, Qianfoshan Hospital, Shandong Province, China.
[Ti] Título:Establishment of a combination scoring method for diagnosis of ocular adnexal lymphoproliferative disease.
[So] Source:PLoS One;12(5):e0160175, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lymphoproliferative diseases (LPDs) of the ocular adnexa encompass the majority of orbital diseases and include reactive follicular hyperplasia (RFH), atypical lymphoid hyperplasia (ALH), and mucosa-associated lymphoid tissue lymphoma (MALToma). Lymphoid follicles (LFs) are usually observed during the histological examination of LPDs. Currently, because there is a lack of specific clinical signs and diagnostic immunohistochemical biomarkers, it is difficult for pathologists to distinguish MALToma from ocular RFH and ALH, which makes the clinical management of these conditions difficult. Here, we analyzed the clinical features of patients with ocular adnexal LPDs (n = 125) and investigated the structure of LFs in paraffin-embedded tissue samples using anti-CD23 and anti-IgD immunochemistry. We found that some clinical features including age, sex, and laterality were different among RFH, LFH, and MALToma. Additionally, immunohistochemistry revealed that the expression of IgD and CD23 was higher in RFH patients and decreased in patients with ALH and MALToma. Moreover, LFs in RFH were intact, whereas the structures of most LFs were disrupted in ALH. In MALToma specimens, few intact LFs were observed. In a further investigation, we combined the results for CD23/IgD immunohistochemistry and the structure of LFs to establish a scoring method for the differential diagnosis of LPDs. According to the BIOMED-2 protocol, we further detected IgH gene monoclonal rearrangement in 73 cases (35 RFH, 17 ALH, and 21 MALToma cases). The sensitivity of our scoring method, based on a comparison with the results of IgH gene monoclonal rearrangement detection, was 85.7% (18/21) for MALToma and 35.3% (6/17) for ALH. Our study provides a method that may be useful for the differential diagnosis of RFH, ALH, and MALToma.
[Mh] Termos MeSH primário: Neoplasias Oculares/diagnóstico
Transtornos Linfoproliferativos/diagnóstico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores
Evolução Clonal/genética
Evolução Clonal/imunologia
Diagnóstico Diferencial
Neoplasias Oculares/genética
Neoplasias Oculares/metabolismo
Feminino
Expressão Gênica
Rearranjo Gênico
Seres Humanos
Cadeias Pesadas de Imunoglobulinas/genética
Imuno-Histoquímica
Transtornos Linfoproliferativos/genética
Transtornos Linfoproliferativos/metabolismo
Masculino
Meia-Idade
Fenótipo
Receptores de IgE/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Immunoglobulin Heavy Chains); 0 (Receptors, IgE)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0160175


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[PMID]:28476932
[Au] Autor:Chhiba KD; Hsu CL; Berdnikovs S; Bryce PJ
[Ad] Endereço:Division of Allergy and Immunology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.
[Ti] Título:Transcriptional Heterogeneity of Mast Cells and Basophils upon Activation.
[So] Source:J Immunol;198(12):4868-4878, 2017 Jun 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mast cells and basophils are developmentally related cells whose activation is a hallmark of allergy. Functionally, mast cells and basophils overlap in their ability to produce several mediators, including histamine and granule proteases, but studies have increasingly demonstrated nonredundant roles. To characterize the transcriptional heterogeneity of mast cells and basophils upon their activation, we performed large-scale comparative microarrays of murine bone marrow-derived mast cells and bone marrow-derived basophils (BMBs) at rest, upon an adaptive-type activation (IgE cross-linking), or upon an innate-type activation (IL-33 stimulation). Hierarchical clustering demonstrated that bone marrow-derived mast cells and BMBs shared specific activation-associated transcriptional signatures but differed in other signatures both between cell type and between activation mode. In bone marrow-derived mast cells, IgE cross-linking upregulated 785 genes, including , , and , whereas IL-33 stimulation induced 823 genes, including , , and Focused bioinformatics pathway analysis demonstrated that IgE activation aligned with processes such as oxidative phosphorylation, angiogenesis, and the p53 pathway. The IL-33-activated transcriptome was enriched in genes commonly altered by NF-κB in response to TNF, by IL-6 via STAT3, and in response to IFN-γ. Furthermore, BMBs activated via IgE cross-linking selectively induced immune response genes , and compared with IL-33-stimulated BMBs. Principal-component analysis revealed key cell- and activation-specific clustering. Overall, our data demonstrate that mast cells and basophils have cell- and activation-specific transcriptional responses and suggest that context-specific gene networks and pathways may shape how the immune system responds to allergens and innate cytokines.
[Mh] Termos MeSH primário: Basófilos/imunologia
Biologia Computacional
Mastócitos/imunologia
Transcrição Genética
[Mh] Termos MeSH secundário: Alérgenos/metabolismo
Animais
Basófilos/metabolismo
Células da Medula Óssea/imunologia
Células Cultivadas
Citocinas/genética
Citocinas/metabolismo
Redes Reguladoras de Genes
Imunoglobulina E/química
Imunoglobulina E/imunologia
Interleucina-33/farmacologia
Interleucinas/genética
Interleucinas/metabolismo
Mastócitos/metabolismo
Camundongos
Receptores de IgE/química
Receptores de IgE/imunologia
Análise Serial de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (Cytokines); 0 (Interleukin-33); 0 (Interleukins); 0 (Receptors, IgE); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601825



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