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[PMID]:28634034
[Au] Autor:Nowak K; Linzner D; Thrasher AJ; Lambert PF; Di WL; Burns SO
[Ad] Endereço:Molecular and Cellular Immunology, Institute of Child Health, University College London, London, UK.
[Ti] Título:Absence of γ-Chain in Keratinocytes Alters Chemokine Secretion, Resulting in Reduced Immune Cell Recruitment.
[So] Source:J Invest Dermatol;137(10):2120-2130, 2017 Oct.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Loss-of-function mutations in the common gamma (γc) chain cytokine receptor subunit give rise to severe combined immunodeficiency characterized by lack of T and natural killer cells and infant death from infection. Hematopoietic stem cell transplantation or gene therapy offer a cure, but despite successful replacement of lymphoid immune lineages, a long-term risk of severe cutaneous human papilloma virus infections persists, possibly related to persistent γc-deficiency in other cell types. Here we show that keratinocytes, the only cell type directly infected by human papilloma virus, express functional γc and its co-receptors. After stimulation with the γc-ligand IL-15, γc-deficient keratinocytes show significantly impaired secretion of specific chemokines including CXCL1, CXCL8, and CCL20, resulting in reduced chemotaxis of dendritic cells and CD4 T cells. Furthermore, γc-deficient keratinocytes also exhibit defective induction of T-cell chemotaxis in a model of stable human papilloma virus-18 infection. These findings suggest that persistent γc-deficiency in keratinocytes alters immune cell recruitment to the skin, which may contribute to the development and persistence of warts in this condition and would require different treatment approaches.
[Mh] Termos MeSH primário: Quimiocinas/genética
Regulação da Expressão Gênica
Doença das Cadeias Pesadas/imunologia
Imunidade Inata
Cadeias gama de Imunoglobulina/metabolismo
Queratinócitos/metabolismo
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Linhagem Celular
Movimento Celular
Quimiocinas/biossíntese
Citometria de Fluxo
Doença das Cadeias Pesadas/genética
Doença das Cadeias Pesadas/metabolismo
Seres Humanos
Queratinócitos/imunologia
Queratinócitos/patologia
RNA/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines); 0 (Immunoglobulin gamma-Chains); 63231-63-0 (RNA)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE


  2 / 1102 MEDLINE  
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[PMID]:28069266
[Au] Autor:Vignon M; Cohen C; Faguer S; Noel LH; Guilbeau C; Rabant M; Higgins S; Hummel A; Hertig A; Francois H; Lequintrec M; Vilaine E; Knebelmann B; Pourrat J; Chauveau D; Goujon JM; Javaugue V; Touchard G; El Karoui K; Bridoux F
[Ad] Endereço:Department of Nephrology, Hôpital Necker Enfants Malades, Université Paris Descartes, Paris, France. Electronic address: marguerite.vignon@aphp.fr.
[Ti] Título:The clinicopathologic characteristics of kidney diseases related to monotypic IgA deposits.
[So] Source:Kidney Int;91(3):720-728, 2017 Mar.
[Is] ISSN:1523-1755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Monoclonal gammopathy of renal significance (MGRS) regroups renal disorders caused by a monoclonal immunoglobulin without overt hematological malignancy. MGRS includes tubular disorders, glomerular disorders with organized deposits, and glomerular disorders with non-organized deposits, such as proliferative glomerulonephritis with monoclonal IgG deposits. Since glomerular involvement related to monotypic IgA deposits is poorly described we performed retrospective analysis and defined clinico-biological characteristics, renal pathology, and outcome in 19 referred patients. This analysis allowed distinction between 2 types of glomerulopathies, α-heavy chain deposition disease (5 patients) and glomerulonephritis with monotypic IgA deposits (14 patients) suggestive of IgA-proliferative glomerulonephritis with monoclonal immunoglobulin deposits in 12 cases. Clinicopathologic characteristics of α-heavy chain deposition disease resemble those of the γ-heavy chain disease, except for a higher frequency of extra-capillary proliferation and extra-renal involvement. IgA-proliferative glomerulonephritis with monoclonal immunoglobulin deposits should be differentiated from diseases with polytypic IgA deposits, given distinct clinical, histological, and pathophysiological features. Similarly to IgG-proliferative glomerulonephritis with monoclonal immunoglobulin deposits, overt hematological malignancy was infrequent, but sensitive serum and bone marrow studies revealed a subtle plasma cell proliferation in most patients with IgA-proliferative glomerulonephritis with monoclonal immunoglobulin deposits. Anti-myeloma agents appeared to favorably influence renal prognosis. Thus, potential progression towards symptomatic IgA multiple myeloma suggests that careful hematological follow-up is mandatory. This series expands the spectrum of renal disease in MGRS.
[Mh] Termos MeSH primário: Glomerulonefrite por IGA/imunologia
Glomerulonefrite/imunologia
Doença das Cadeias Pesadas/imunologia
Imunoglobulina A/análise
Rim/imunologia
Mieloma Múltiplo/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores/análise
Biópsia
Proliferação Celular
Diagnóstico Diferencial
Progressão da Doença
Feminino
Imunofluorescência
França
Glomerulonefrite/tratamento farmacológico
Glomerulonefrite/patologia
Glomerulonefrite por IGA/tratamento farmacológico
Glomerulonefrite por IGA/patologia
Doença das Cadeias Pesadas/tratamento farmacológico
Doença das Cadeias Pesadas/patologia
Seres Humanos
Cadeias alfa de Imunoglobulina/análise
Cadeias gama de Imunoglobulina/análise
Rim/efeitos dos fármacos
Rim/ultraestrutura
Masculino
Meia-Idade
Mieloma Múltiplo/tratamento farmacológico
Mieloma Múltiplo/patologia
Valor Preditivo dos Testes
Prognóstico
Estudos Retrospectivos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (Immunoglobulin A); 0 (Immunoglobulin alpha-Chains); 0 (Immunoglobulin gamma-Chains); 0 (heavy chain disease proteins, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170111
[St] Status:MEDLINE


  3 / 1102 MEDLINE  
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[PMID]:27750045
[Au] Autor:Slot LM; Hoogeboom R; Smit LA; Wormhoudt TA; Biemond BJ; Oud ME; Schilder-Tol EJ; Mulder AB; Jongejan A; van Kampen AH; Kluin PM; Guikema JE; Bende RJ; van Noesel CJ
[Ad] Endereço:Department of Pathology, Academic Medical Center Amsterdam, Amsterdam, the Netherlands; Lymphoma and Myeloma Center Amsterdam (LYMMCARE), Amsterdam, the Netherlands.
[Ti] Título:B-Lymphoblastic Lymphomas Evolving from Follicular Lymphomas Co-Express Surrogate Light Chains and Mutated Gamma Heavy Chains.
[So] Source:Am J Pathol;186(12):3273-3284, 2016 Dec.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Follicular lymphoma (FL) is an indolent B-cell non-Hodgkin lymphoma able to transform into germinal center-type diffuse large B-cell lymphoma. We describe four extraordinary cases of FL, which progressed to TdT CD20 precursor B-lymphoblastic lymphoma (B-LBL). Fluorescence in situ hybridization analysis showed that all four B-LBLs had acquired a MYC translocation on transformation. Comparative genomic hybridization analysis of one case demonstrated that in addition to 26 numerical aberrations that were shared between the FL and B-LBL, deletion of CDKN2A/B and 17q11, 14q32 amplification, and copy-neutral loss of heterozygosity of 9p were gained in the B-LBL cells. Whole-exome sequencing revealed mutations in FMN2, NEB, and SYNE1 and a nonsense mutation in KMT2D, all shared by the FL and B-LBL, and TNFRSF14, SMARCA2, CCND3 mutations uniquely present in the B-LBL. Remarkably, all four FL-B-LBL pairs expressed IgG. In two B-LBLs, evidence was obtained for ongoing rearrangement of IG light chain variable genes and expression of the surrogate light chain. IGHV mutation analysis showed that all FL-B-LBL pairs harbored identical or near-identical somatic mutations. From the somatic gene alterations found in the IG and non-IG genes, we conclude that the FLs and B-LBLs did not develop in parallel from early t(14;18)-positive IG-unmutated precursors, but that the B-LBLs developed from preexistent FL subclones that accumulated additional genetic damage.
[Mh] Termos MeSH primário: Cadeias Leves Substitutas da Imunoglobulina/genética
Cadeias gama de Imunoglobulina/genética
Linfoma de Células B/genética
Linfoma Folicular/genética
[Mh] Termos MeSH secundário: Linfócitos B/patologia
Hibridização Genômica Comparativa
Ciclina D3/genética
Inibidor de Quinase Dependente de Ciclina p15/genética
Inibidor de Quinase Dependente de Ciclina p18/genética
Análise Mutacional de DNA
Feminino
Centro Germinativo/patologia
Seres Humanos
Cadeias Leves Substitutas da Imunoglobulina/metabolismo
Cadeias gama de Imunoglobulina/metabolismo
Hibridização in Situ Fluorescente
Linfoma de Células B/patologia
Linfoma Folicular/patologia
Masculino
Meia-Idade
Mutação
Neurofibromina 1/genética
Membro 14 de Receptores do Fator de Necrose Tumoral/genética
Fatores de Transcrição/genética
Translocação Genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCND3 protein, human); 0 (CDKN2A protein, human); 0 (CDKN2B protein, human); 0 (Cyclin D3); 0 (Cyclin-Dependent Kinase Inhibitor p15); 0 (Cyclin-Dependent Kinase Inhibitor p18); 0 (Immunoglobulin Light Chains, Surrogate); 0 (Immunoglobulin gamma-Chains); 0 (Neurofibromin 1); 0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (SMARCA2 protein, human); 0 (TNFRSF14 protein, human); 0 (Transcription Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE


  4 / 1102 MEDLINE  
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[PMID]:27623628
[Au] Autor:Zhai L; Zhao Y; Peng S; Zhu K; Yu R; Chen H; Lin T; Lin L
[Ad] Endereço:Department of Medical Oncology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510405, Guangdong, People's Republic of China.
[Ti] Título:Detection of the value of consecutive serum total light chain (sTLC) in patients diagnosed with diffuse large B cell lymphoma.
[So] Source:Ann Hematol;95(12):1999-2007, 2016 Dec.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:There are limited data on serum total light chain (sTLC) in lymphoma and its relative role on the outcome of diffuse large B cell lymphoma (DLBCL) patients. Blood samples from 46 cases newly diagnosed with DLBCL were collected consecutively during chemotherapy to detect sTLC, IgG, IgA, and IgM levels. Clinical data and survival outcomes were analyzed according to the results of sTLC measurements. In summary, 22 patients (47.8 %) had abnormal k or λ light chain, respectively, and 6 patients (13.0 %) had both abnormal k and λ light chains before chemotherapy. Patients with elevated k light chain more frequently displayed multiple extra-nodal organ involvement (P = 0.01) and had an inferior overall survival (OS) (P = 0.041) and progression-free survival (PFS) (P = 0.044) compared to patients with normal level of k light chain. Furthermore, patients with elevated level of both k and λ also exhibited significant association with shorter OS (P = 0.002) and PFS (P = 0.009). Both elevated k alone and concurrent elevated k and λ had independent adverse effects on PFS (P = 0.031 and P = 0.019, respectively). sTLC level was reduced gradually by treatment in this study and reached the lowest point after the fourth cycle of chemotherapy, which was consistent with the disease behavior during chemotherapy. Considering the small sample size of this study, these results should be confirmed in a larger prospective study.
[Mh] Termos MeSH primário: Cadeias gama de Imunoglobulina/sangue
Cadeias kappa de Imunoglobulina/sangue
Linfoma Difuso de Grandes Células B/sangue
Linfoma Difuso de Grandes Células B/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Anticorpos Monoclonais Murinos/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Biomarcadores/sangue
Ciclofosfamida/administração & dosagem
Doxorrubicina/administração & dosagem
Feminino
Seguimentos
Seres Humanos
Linfoma Difuso de Grandes Células B/tratamento farmacológico
Masculino
Meia-Idade
Prednisona/administração & dosagem
Vincristina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Murine-Derived); 0 (Biomarkers); 0 (Immunoglobulin gamma-Chains); 0 (Immunoglobulin kappa-Chains); 0 (R-CHOP protocol); 5J49Q6B70F (Vincristine); 80168379AG (Doxorubicin); 8N3DW7272P (Cyclophosphamide); VB0R961HZT (Prednisone)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170127
[Lr] Data última revisão:
170127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160915
[St] Status:MEDLINE


  5 / 1102 MEDLINE  
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[PMID]:26884373
[Au] Autor:Jin H; Ni X; Deng R; Song Q; Young J; Cassady K; Zhang M; Forman S; Martin PJ; Liu Q; Zeng D
[Ad] Endereço:Departments of Diabetes Research and Hematology/Hematopoietic Cell Transplantation, The Beckman Research Institute of City-Hope, Duarte, CA; Department of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, China;
[Ti] Título:Antibodies from donor B cells perpetuate cutaneous chronic graft-versus-host disease in mice.
[So] Source:Blood;127(18):2249-60, 2016 May 05.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cutaneous sclerosis is one of the most common clinical manifestations of chronic graft-versus-host disease (cGVHD). Donor CD4(+) T and B cells play important roles in cGVHD pathogenesis, but the role of antibodies from donor B cells remains unclear. In the current studies, we generated immunoglobulin (Ig)H(µÎ³1) DBA/2 mice whose B cells have normal antigen-presentation and regulatory functions but cannot secrete antibodies. With a murine cGVHD model using DBA/2 donors and BALB/c recipients, we have shown that wild-type (WT) grafts induce persistent cGVHD with damage in the thymus, peripheral lymphoid organs, and skin, as well as cutaneous T helper 17 cell (Th17) infiltration. In contrast, IgH(µÎ³1) grafts induced only transient cGVHD with little damage in the thymus or peripheral lymph organs or with little cutaneous Th17 infiltration. Injections of IgG-containing sera from cGVHD recipients given WT grafts but not IgG-deficient sera from recipients given IgH(µÎ³1) grafts led to deposition of IgG in the thymus and skin, with resulting damage in the thymus and peripheral lymph organs, cutaneous Th17 infiltration, and perpetuation of cGVHD in recipients given IgH(µÎ³1) grafts. These results indicate that donor B-cell antibodies augment cutaneous cGVHD in part by damaging the thymus and increasing tissue infiltration of pathogenic Th17 cells.
[Mh] Termos MeSH primário: Subpopulações de Linfócitos B/imunologia
Doença Enxerto-Hospedeiro/imunologia
Isoanticorpos/imunologia
[Mh] Termos MeSH secundário: Animais
Subpopulações de Linfócitos B/secreção
Subpopulações de Linfócitos B/transplante
Quimiocina CCL20/secreção
Doença Crônica
Células Dendríticas/secreção
Doença Enxerto-Hospedeiro/patologia
Imunoglobulina G/análise
Cadeias Pesadas de Imunoglobulinas
Cadeias gama de Imunoglobulina/genética
Cadeias gama de Imunoglobulina/imunologia
Cadeias mu de Imunoglobulina/genética
Cadeias mu de Imunoglobulina/imunologia
Interleucina-23/secreção
Tecido Linfoide/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos DBA
Quimera por Radiação
Pele/patologia
Organismos Livres de Patógenos Específicos
Células Th17/imunologia
Timo/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL20 protein, mouse); 0 (Chemokine CCL20); 0 (Immunoglobulin G); 0 (Immunoglobulin Heavy Chains); 0 (Immunoglobulin gamma-Chains); 0 (Immunoglobulin mu-Chains); 0 (Interleukin-23); 0 (Isoantibodies)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160218
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2015-09-668145


  6 / 1102 MEDLINE  
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[PMID]:26875967
[Au] Autor:Iijima M; Sekiguchi N; Nagata A; Wagatsuma M; Midorikawa K; Kurimoto M; Noto S; Yamada K; Takezako N
[Ad] Endereço:Hematology Division, National Hospital Organization Disaster Medical Center, Japan.
[Ti] Título:Gamma Heavy Chain Disease with T-cell Large Granular Lymphocytic Leukemia: A Case Report and Review of the Literature.
[So] Source:Intern Med;55(4):399-403, 2016.
[Is] ISSN:1349-7235
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Gamma heavy chain disease (gHCD) is a rare lymphoproliferative disorder characterized by the production of a truncated immunoglobulin heavy chain. Although some cases of gHCD are concurrent with other lymphoid neoplasms, few have been reported. We herein present the case of a 73-year-old woman with gHCD and T-cell large granular lymphocytic leukemia. A multiparameter flow cytometry analysis revealed neoplastic cells that were positive for CD28, a marker of T-cell activation, the anti-apoptotic antigen of neoplastic plasma cells, CD38 and CD45. The results of this multiparameter flow cytometry analysis may contribute to furthering the understanding of the clinicopathological features of gHCD.
[Mh] Termos MeSH primário: Anemia/imunologia
Fadiga/imunologia
Doença das Cadeias Pesadas/patologia
Cadeias gama de Imunoglobulina/metabolismo
Leucemia Linfocítica Granular Grande/patologia
Linfócitos/metabolismo
[Mh] Termos MeSH secundário: Idoso
Anemia/etiologia
Análise Citogenética
Fadiga/etiologia
Feminino
Citometria de Fluxo
Doença das Cadeias Pesadas/complicações
Doença das Cadeias Pesadas/imunologia
Seres Humanos
Cadeias Pesadas de Imunoglobulinas
Cadeias gama de Imunoglobulina/sangue
Leucemia Linfocítica Granular Grande/complicações
Leucemia Linfocítica Granular Grande/imunologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunoglobulin Heavy Chains); 0 (Immunoglobulin gamma-Chains)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160215
[Lr] Data última revisão:
160215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160216
[St] Status:MEDLINE
[do] DOI:10.2169/internalmedicine.55.5042


  7 / 1102 MEDLINE  
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[PMID]:26439167
[Au] Autor:Sato M; Oiso N; Shiga T; Morita R; Kimura M; Funauchi M; Matsumura I; Kawada A
[Ad] Endereço:Department of Dermatology, Kinki University Faculty of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511, Japan.
[Ti] Título:Cryoglobulinaemia (IgG-κ-type and IgM-γ-type) with Occluding Leukocytoclastic Vasculitis in a Patient with Vitiligo and Demyelinating Polyneuropathy.
[So] Source:Acta Derm Venereol;96(4):568-9, 2016 May.
[Is] ISSN:1651-2057
[Cp] País de publicação:Sweden
[La] Idioma:eng
[Mh] Termos MeSH primário: Crioglobulinemia/imunologia
Síndrome de Guillain-Barré/imunologia
Imunoglobulina G/imunologia
Imunoglobulina M/imunologia
Cadeias gama de Imunoglobulina/imunologia
Cadeias kappa de Imunoglobulina/imunologia
Vasculite Leucocitoclástica Cutânea/imunologia
Vitiligo/imunologia
[Mh] Termos MeSH secundário: Biópsia
Crioglobulinemia/complicações
Crioglobulinemia/diagnóstico
Crioglobulinemia/tratamento farmacológico
Glucocorticoides/uso terapêutico
Síndrome de Guillain-Barré/diagnóstico
Síndrome de Guillain-Barré/tratamento farmacológico
Seres Humanos
Imunoglobulina G/sangue
Imunoglobulina M/sangue
Cadeias gama de Imunoglobulina/sangue
Cadeias kappa de Imunoglobulina/sangue
Masculino
Meia-Idade
Resultado do Tratamento
Vasculite Leucocitoclástica Cutânea/diagnóstico
Vasculite Leucocitoclástica Cutânea/tratamento farmacológico
Vitiligo/diagnóstico
Vitiligo/tratamento farmacológico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucocorticoids); 0 (Immunoglobulin G); 0 (Immunoglobulin M); 0 (Immunoglobulin gamma-Chains); 0 (Immunoglobulin kappa-Chains)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170117
[Lr] Data última revisão:
170117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151007
[St] Status:MEDLINE
[do] DOI:10.2340/00015555-2250


  8 / 1102 MEDLINE  
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[PMID]:26536348
[Au] Autor:Simpson HM; Khan RZ; Song C; Sharma D; Sadashivaiah K; Furusawa A; Liu X; Nagaraj S; Sengamalay N; Sadzewicz L; Tallon LJ; Chen QC; Livak F; Rapoport AP; Kimball A; Banerjee A
[Ad] Endereço:Program in Oncology, Greenebaum Cancer Center, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, United States of America.
[Ti] Título:Concurrent Mutations in ATM and Genes Associated with Common γ Chain Signaling in Peripheral T Cell Lymphoma.
[So] Source:PLoS One;10(11):e0141906, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peripheral T cell lymphoma (PTCL) is a heterogeneous malignancy with poor response to current therapeutic strategies and incompletely characterized genetics. We conducted whole exome sequencing of matched PTCL and non-malignant samples from 12 patients, spanning 8 subtypes, to identify potential oncogenic mutations in PTCL. Analysis of the mutations identified using computational algorithms, CHASM, PolyPhen2, PROVEAN, and MutationAssessor to predict the impact of these mutations on protein function and PTCL tumorigenesis, revealed 104 somatic mutations that were selected as high impact by all four algorithms. Our analysis identified recurrent somatic missense or nonsense mutations in 70 genes, 9 of which contained mutations predicted significant by all 4 algorithms: ATM, RUNX1T1, WDR17, NTRK3, TP53, TRMT12, CACNA2D1, INTS8, and KCNH8. We observed somatic mutations in ATM (ataxia telangiectasia-mutated) in 5 out of the 12 samples and mutations in the common gamma chain (γc) signaling pathway (JAK3, IL2RG, STAT5B) in 3 samples, all of which also harbored mutations in ATM. Our findings contribute insights into the genetics of PTCL and suggest a relationship between γc signaling and ATM in T cell malignancy.
[Mh] Termos MeSH primário: Proteínas Mutadas de Ataxia Telangiectasia/genética
Cadeias gama de Imunoglobulina/genética
Linfoma de Células T Periférico/genética
Mutação/genética
Proteínas Supressoras de Tumor/genética
[Mh] Termos MeSH secundário: Algoritmos
Exoma/genética
Feminino
Citometria de Fluxo
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Immunoglobulin gamma-Chains); 0 (Tumor Suppressor Proteins); EC 2.7.11.1 (ATM protein, human); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170412
[Lr] Data última revisão:
170412
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151105
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0141906


  9 / 1102 MEDLINE  
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[PMID]:26436649
[Au] Autor:Quast I; Keller CW; Maurer MA; Giddens JP; Tackenberg B; Wang LX; Münz C; Nimmerjahn F; Dalakas MC; Lünemann JD
[Ti] Título:Sialylation of IgG Fc domain impairs complement-dependent cytotoxicity.
[So] Source:J Clin Invest;125(11):4160-70, 2015 Nov 02.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IgG molecules exert both pro- and antiinflammatory effector functions based on the composition of the fragment crystallizable (Fc) domain glycan. Sialylated IgG Fc domains have antiinflammatory properties that are attributed to their ability to increase the activation threshold of innate effector cells to immune complexes by stimulating the upregulation of the inhibitory Fcγ receptor IIB (FcγRIIB). Here, we report that IgG Fc sialylation of human monoclonal IgG1 molecules impairs their efficacy to induce complement-mediated cytotoxicity (CDC). Fc sialylation of a CD20-targeting antibody had no impact on antibody-dependent cellular cytotoxicity and did not change the affinity of the antibody for activating Fcγ receptors. In contrast, the presence of sialic acid abrogated the increased binding of C1q to Fc-galactosylated IgG1 and resulted in decreased levels of C3b deposition on the cell surface. Similar to monoclonal antibodies, sialic acid inhibited the increased C1q binding to galactosylated Fc fragments in human polyclonal IgG. In sera derived from patients with chronic inflammatory demyelinating polyneuropathy, an autoimmune disease of the peripheral nervous system in which humoral immune responses mediate tissue damage, induction of IgG Fc sialylation was associated with clinical disease remission. Thus, impairment of CDC represents an FcγR-independent mechanism by which Fc-sialylated glycovariants might limit proinflammatory IgG effector functions.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Via Clássica do Complemento
Proteínas do Sistema Complemento/imunologia
Imunoglobulina G/química
Cadeias gama de Imunoglobulina/química
Ácido N-Acetilneuramínico/química
Rituximab/química
[Mh] Termos MeSH secundário: Animais
Citotoxicidade Celular Dependente de Anticorpos
Antígenos CD20/imunologia
Linfoma de Burkitt/patologia
Linhagem Celular Tumoral
Complemento C1q/imunologia
Complemento C1q/metabolismo
Citotoxicidade Imunológica
Glicosilação
Seres Humanos
Imunoglobulina G/imunologia
Cadeias gama de Imunoglobulina/imunologia
Imunoglobulinas Intravenosas/uso terapêutico
Células Matadoras Naturais/imunologia
Depleção Linfocítica
Camundongos
Glicoproteína Mielina-Oligodendrócito/imunologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/imunologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/terapia
Processamento de Proteína Pós-Traducional
Receptores de IgG/imunologia
Rituximab/imunologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD20); 0 (Immunoglobulin G); 0 (Immunoglobulin gamma-Chains); 0 (Immunoglobulins, Intravenous); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Receptors, IgG); 4F4X42SYQ6 (Rituximab); 80295-33-6 (Complement C1q); 9007-36-7 (Complement System Proteins); GZP2782OP0 (N-Acetylneuraminic Acid)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:151006
[St] Status:MEDLINE


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[PMID]:26096419
[Au] Autor:Pallavi R
[Ad] Endereço:Department of Hematology and Oncology, Westchester Medical Center, New York Medical College, Valhalla, New York.
[Ti] Título:Abdominal "Heaviness".
[So] Source:J Am Geriatr Soc;63(6):1277-8, 2015 Jun.
[Is] ISSN:1532-5415
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Doença das Cadeias Pesadas/complicações
Doença das Cadeias Pesadas/diagnóstico
[Mh] Termos MeSH secundário: Idoso de 80 Anos ou mais
Doença das Cadeias Pesadas/terapia
Seres Humanos
Cadeias gama de Imunoglobulina
Masculino
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Immunoglobulin gamma-Chains)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:150622
[Lr] Data última revisão:
150622
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150623
[St] Status:MEDLINE
[do] DOI:10.1111/jgs.13518



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