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[PMID]:29179214
[Au] Autor:Wang L; Wei Y; Fang W; Lu C; Chen J; Cui G; Diao H
[Ad] Endereço:State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
[Ti] Título:Cetuximab Enhanced the Cytotoxic Activity of Immune Cells during Treatment of Colorectal Cancer.
[So] Source:Cell Physiol Biochem;44(3):1038-1050, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Cetuximab is a chimeric IgG1 monoclonal antibody which targets the extracellular domain of epidermal growth factor receptor. This antibody is widely used for colorectal cancer (CRC) treatment but its influence on the immune system is incompletely understood. METHODS: The immune influence of cetuximab therapy in CRC patients was investigated by analyzing peripheral blood mononuclear cells using flow cytometry. We undertook in vitro cytotoxicity and cytokine-profile assays to ascertain the immunomodulatory effect of cetuximab treatment. RESULTS: The number of CD3+ T, CD8+ T, and natural killer (NK) cells was increased significantly and T-regulatory cells reduced gradually after cetuximab treatment. Percentage of CD4+ T, natural killer T (NKT)-like, invariant NKT, and dendritic cells was similar between baseline patients and cetuximab patients. Expression of CD137 on NK and CD8+ T cells was increased significantly after 4 weeks of cetuximab therapy. In vitro cetuximab treatment markedly increased expression of CD137 and CD107a on NK and CD8+ T cells. Cetuximab treatment promoted the cytotoxic activity of NK and CD8+ T cells against tumor cells. CONCLUSION: Cetuximab treatment promotes activation of the immune response but alleviates immunosuppression: this might be the underlying anti-CRC effect of cetuximab.
[Mh] Termos MeSH primário: Antineoplásicos Imunológicos/uso terapêutico
Cetuximab/uso terapêutico
Neoplasias Colorretais/tratamento farmacológico
Linfócitos/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Antineoplásicos Imunológicos/farmacologia
Linfócitos T CD4-Positivos/citologia
Linfócitos T CD4-Positivos/efeitos dos fármacos
Linfócitos T CD4-Positivos/metabolismo
Linfócitos T CD8-Positivos/citologia
Linfócitos T CD8-Positivos/efeitos dos fármacos
Linfócitos T CD8-Positivos/metabolismo
Células Cultivadas
Cetuximab/farmacologia
Neoplasias Colorretais/patologia
Citocinas/sangue
Feminino
Células HT29
Seres Humanos
Células K562
Células Matadoras Naturais/citologia
Células Matadoras Naturais/efeitos dos fármacos
Células Matadoras Naturais/metabolismo
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/metabolismo
Linfócitos/citologia
Linfócitos/efeitos dos fármacos
Proteína 1 de Membrana Associada ao Lisossomo/metabolismo
Masculino
Meia-Idade
Linfócitos T Reguladores/citologia
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/metabolismo
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Immunological); 0 (Cytokines); 0 (Lysosomal-Associated Membrane Protein 1); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 9); PQX0D8J21J (Cetuximab)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485404


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[PMID]:28877989
[Au] Autor:Madireddi S; Eun SY; Mehta AK; Birta A; Zajonc DM; Niki T; Hirashima M; Podack ER; Schreiber TH; Croft M
[Ad] Endereço:Division of Immune Regulation, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037.
[Ti] Título:Regulatory T Cell-Mediated Suppression of Inflammation Induced by DR3 Signaling Is Dependent on Galectin-9.
[So] Source:J Immunol;199(8):2721-2728, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stimulation of several TNF receptor family proteins has been shown to dampen inflammatory disease in murine models through augmenting the number and/or activity of regulatory T cells (Tregs). We recently found that one molecule, 4-1BB, used binding to Galectin-9 to exert its immunosuppressive effects and drive expansion of CD8 Foxp3 Tregs. We now show that ligation of another TNFR family molecule, DR3, which has previously been found to strongly expand CD4 Foxp3 Tregs and suppress inflammation, also requires Galectin-9. We found that the extracellular region of DR3 directly binds to Galectin-9, and that Galectin-9 associates with DR3 in Tregs. From studies in vitro with Galectin-9 CD4 T cells and Tregs, we found that stimulatory activity induced by ligating DR3 was in part dependent on Galectin-9. In vivo, in a model of experimental autoimmune encephalomyelitis, we show that an agonist of DR3 suppressed disease, correlating with expansion of CD4 Foxp3 Tregs, and this protective effect was lost in Galectin-9 mice. Similar results were seen in an allergic lung inflammation model. Thus, we demonstrate a novel function of Galectin-9 in facilitating activity of DR3 related to Treg-mediated suppression.
[Mh] Termos MeSH primário: Encefalomielite Autoimune Experimental/imunologia
Galectinas/metabolismo
Inflamação/imunologia
Esclerose Múltipla/imunologia
Subpopulações de Linfócitos T/imunologia
Linfócitos T Reguladores/imunologia
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Células Cultivadas
Fatores de Transcrição Forkhead/metabolismo
Galectinas/genética
Seres Humanos
Tolerância Imunológica
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Ligação Proteica
Membro 25 de Receptores de Fatores de Necrose Tumoral/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Galectins); 0 (Receptors, Tumor Necrosis Factor, Member 25); 0 (Tnfrsf25 protein, mouse); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 9); 0 (galectin 9, mouse)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700575


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[PMID]:28789924
[Au] Autor:Mbanwi AN; Lin GHY; Wang KC; Watts TH
[Ad] Endereço:Department of Immunology, University of Toronto, Toronto, ON M5S1A8, Canada.
[Ti] Título:Constitutive interaction between 4-1BB and 4-1BBL on murine LPS-activated bone marrow dendritic cells masks detection of 4-1BBL by TKS-1 but not 19H3 antibody.
[So] Source:J Immunol Methods;450:81-89, 2017 Nov.
[Is] ISSN:1872-7905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:4-1BB is a TNFR family member associated with NF-κB mediated survival signaling. 4-1BB is widely expressed on activated cells of the immune system, including activated T cells, NK cells and dendritic cells. Its ligand, 4-1BBL, is transiently expressed on activated antigen presenting cells and at low levels on activated T cells. Although 4-1BBL-deficient mice clearly demonstrate a role for 4-1BBL in CD8 T cell responses to viruses such as influenza, 4-1BBL can be difficult to detect following infection of mice. Here we provide evidence for a constitutive interaction between endogenous 4-1BB and 4-1BBL on LPS activated bone marrow-derived murine dendritic cells that can mask its detection, with implications for measurement of 4-1BBL expression. The masking of 4-1BBL by its receptor results in loss of reactivity to the anti-4-1BBL antibody TKS-1, whereas the 19H3 antibody binds to 4-1BBL in the presence or absence of 4-1BB. Moreover, 4-1BB/4-1BBL interaction can occur in trans between 4-1BB and 4-1BB dendritic cells in culture. These data suggest that 19H3 is the preferable antibody to use to detect 4-1BBL in the presence of its receptor.
[Mh] Termos MeSH primário: Ligante 4-1BB/imunologia
Anticorpos/imunologia
Células da Medula Óssea/efeitos dos fármacos
Separação Celular/métodos
Células Dendríticas/efeitos dos fármacos
Citometria de Fluxo
Lipopolissacarídeos/farmacologia
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Mh] Termos MeSH secundário: Ligante 4-1BB/genética
Ligante 4-1BB/metabolismo
Animais
Especificidade de Anticorpos
Células da Medula Óssea/imunologia
Células da Medula Óssea/metabolismo
Células Cultivadas
Células Dendríticas/imunologia
Células Dendríticas/metabolismo
Epitopos
Genótipo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fenótipo
Ligação Proteica
Reprodutibilidade dos Testes
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-1BB Ligand); 0 (Antibodies); 0 (Epitopes); 0 (Lipopolysaccharides); 0 (Tnfrsf9 protein, mouse); 0 (Tnfsf9 protein, mouse); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 9)
[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:170810
[St] Status:MEDLINE


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[PMID]:28628092
[Au] Autor:Ganesan AP; Clarke J; Wood O; Garrido-Martin EM; Chee SJ; Mellows T; Samaniego-Castruita D; Singh D; Seumois G; Alzetani A; Woo E; Friedmann PS; King EV; Thomas GJ; Sanchez-Elsner T; Vijayanand P; Ottensmeier CH
[Ad] Endereço:La Jolla Institute for Allergy &Immunology, La Jolla, California, USA.
[Ti] Título:Tissue-resident memory features are linked to the magnitude of cytotoxic T cell responses in human lung cancer.
[So] Source:Nat Immunol;18(8):940-950, 2017 Aug.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Therapies that boost the anti-tumor responses of cytotoxic T lymphocytes (CTLs) have shown promise; however, clinical responses to the immunotherapeutic agents currently available vary considerably, and the molecular basis of this is unclear. We performed transcriptomic profiling of tumor-infiltrating CTLs from treatment-naive patients with lung cancer to define the molecular features associated with the robustness of anti-tumor immune responses. We observed considerable heterogeneity in the expression of molecules associated with activation of the T cell antigen receptor (TCR) and of immunological-checkpoint molecules such as 4-1BB, PD-1 and TIM-3. Tumors with a high density of CTLs showed enrichment for transcripts linked to tissue-resident memory cells (T cells), such as CD103, and CTLs from CD103 tumors displayed features of enhanced cytotoxicity. A greater density of T cells in tumors was predictive of a better survival outcome in lung cancer, and this effect was independent of that conferred by CTL density. Here we define the 'molecular fingerprint' of tumor-infiltrating CTLs and identify potentially new targets for immunotherapy.
[Mh] Termos MeSH primário: Adenocarcinoma/imunologia
Carcinoma de Células Escamosas/imunologia
Neoplasias de Cabeça e Pescoço/imunologia
Memória Imunológica/imunologia
Neoplasias Pulmonares/imunologia
Linfócitos do Interstício Tumoral/imunologia
Linfócitos T Citotóxicos/imunologia
[Mh] Termos MeSH secundário: Adenocarcinoma/mortalidade
Adulto
Idoso
Idoso de 80 Anos ou mais
Antígenos CD/genética
Carcinoma de Células Escamosas/mortalidade
Feminino
Perfilação da Expressão Gênica
Receptor Celular 2 do Vírus da Hepatite A/genética
Seres Humanos
Imunoterapia
Cadeias alfa de Integrinas/genética
Neoplasias Pulmonares/mortalidade
Linfócitos do Interstício Tumoral/metabolismo
Masculino
Meia-Idade
Prognóstico
Receptor de Morte Celular Programada 1/genética
Receptores de Antígenos de Linfócitos T/genética
Taxa de Sobrevida
Linfócitos T Citotóxicos/metabolismo
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (HAVCR2 protein, human); 0 (Hepatitis A Virus Cellular Receptor 2); 0 (Integrin alpha Chains); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Antigen, T-Cell); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 9); 0 (alpha E integrins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3775


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[PMID]:28545292
[Au] Autor:Yin YJ; Yang S; Chen YC
[Ti] Título:[Role of ubiquitin proteasome system in CD137 signaling-mediated atherosclerosis].
[So] Source:Zhonghua Xin Xue Guan Bing Za Zhi;45(4):349-352, 2017 Apr 24.
[Is] ISSN:0253-3758
[Cp] País de publicação:China
[La] Idioma:chi
[Mh] Termos MeSH primário: Aterosclerose
Complexo de Endopeptidases do Proteassoma
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral
Ubiquitina
[Mh] Termos MeSH secundário: Seres Humanos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Necrosis Factor Receptor Superfamily, Member 9); 0 (Ubiquitin); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0253-3758.2017.04.021


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[PMID]:28523432
[Au] Autor:Liu X; Jiang S; Fang C; Li H; Zhang X; Zhang F; June CH; Zhao Y
[Ad] Endereço:Key Laboratory for Experimental Teratology of Ministry of Education and Department of Immunology, School of Basic Medical Sciences, Shandong University, Jinan, 250012, China.
[Ti] Título:Novel T cells with improved in vivo anti-tumor activity generated by RNA electroporation.
[So] Source:Protein Cell;8(7):514-526, 2017 Jul.
[Is] ISSN:1674-8018
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The generation of T cells with maximal anti-tumor activities will significantly impact the field of T-cell-based adoptive immunotherapy. In this report, we found that OKT3/IL-2-stimulated T cells were phenotypically more heterogeneous, with enhanced anti-tumor activity in vitro and when locally administered in a solid tumor mouse model. To further improve the OKT3/IL-2-based T cell manufacturing procedure, we developed a novel T cell stimulation and expansion method in which peripheral blood mononuclear cells were electroporated with mRNA encoding a chimeric membrane protein consisting of a single-chain variable fragment against CD3 and the intracellular domains of CD28 and 4-1BB (OKT3-28BB). The expanded T cells were phenotypically and functionally similar to T cells expanded by OKT3/IL-2. Moreover, co-electroporation of CD86 and 4-1BBL could further change the phenotype and enhance the in vivo anti-tumor activity. Although T cells expanded by the co-electroporation of OKT3-28BB with CD86 and 4-1BBL showed an increased central memory phenotype, the T cells still maintained tumor lytic activities as potent as those of OKT3/IL-2 or OKT3-28BB-stimulated T cells. In different tumor mouse models, T cells expanded by OKT3-28BB RNA electroporation showed anti-tumor activities superior to those of OKT3/IL-2 T cells. Hence, T cells with both a less differentiated phenotype and potent tumor killing ability can be generated by RNA electroporation, and this T cell manufacturing procedure can be further optimized by simply co-delivering other splices of RNA, thus providing a simple and cost-effective method for generating high-quality T cells for adoptive immunotherapy.
[Mh] Termos MeSH primário: Antígenos CD28
Eletroporação
Imunidade Celular
Neoplasias Experimentais/imunologia
RNA Mensageiro
Linfócitos T/imunologia
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral
[Mh] Termos MeSH secundário: Animais
Antígenos CD28/genética
Antígenos CD28/imunologia
Seres Humanos
Interleucina-2/imunologia
Células K562
Camundongos
Muromonab-CD3/imunologia
Neoplasias Experimentais/genética
Neoplasias Experimentais/patologia
RNA Mensageiro/genética
RNA Mensageiro/imunologia
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD28 Antigens); 0 (Interleukin-2); 0 (Muromonab-CD3); 0 (RNA, Messenger); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 9)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE
[do] DOI:10.1007/s13238-017-0422-6


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[PMID]:28404636
[Au] Autor:Cleary KLS; Chan HTC; James S; Glennie MJ; Cragg MS
[Ad] Endereço:Antibody and Vaccine Group, Cancer Sciences Unit, Faculty of Medicine, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, United Kingdom.
[Ti] Título:Antibody Distance from the Cell Membrane Regulates Antibody Effector Mechanisms.
[So] Source:J Immunol;198(10):3999-4011, 2017 May 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immunotherapy using mAbs, such as rituximab, is an established means of treating hematological malignancies. Abs can elicit a number of mechanisms to delete target cells, including complement-dependent cytotoxicity, Ab-dependent cellular cytotoxicity, and Ab-dependent cellular phagocytosis. The inherent properties of the target molecule help to define which of these mechanisms are more important for efficacy. However, it is often unclear why mAb binding to different epitopes within the same target elicits different levels of therapeutic activity. To specifically address whether distance from the target cell membrane influences the aforementioned effector mechanisms, a panel of fusion proteins consisting of a CD20 or CD52 epitope attached to various CD137 scaffold molecules was generated. The CD137 scaffold was modified through the removal or addition of cysteine-rich extracellular domains to produce a panel of chimeric molecules that held the target epitope at different distances along the protein. It was shown that complement-dependent cytotoxicity and Ab-dependent cellular cytotoxicity favored a membrane-proximal epitope, whereas Ab-dependent cellular phagocytosis favored an epitope positioned further away. These findings were confirmed using reagents targeting the membrane-proximal or -distal domains of CD137 itself before investigating these properties in vivo, where a clear difference in the splenic clearance of transfected tumor cells was observed. Together, this work demonstrates how altering the position of the Ab epitope is able to change the effector mechanisms engaged and facilitates the selection of mAbs designed to delete target cells through specific effector mechanisms and provide more effective therapeutic agents.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Citotoxicidade Celular Dependente de Anticorpos
Membrana Celular/imunologia
Epitopos/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/genética
Anticorpos Monoclonais Murinos/imunologia
Antígenos CD/genética
Antígenos CD/imunologia
Antígenos CD20/genética
Antígenos CD20/imunologia
Antígenos de Neoplasias/genética
Antígenos de Neoplasias/imunologia
Antígeno CD52
Linhagem Celular Tumoral
Glicoproteínas/genética
Glicoproteínas/imunologia
Seres Humanos
Imunoterapia
Camundongos
Fagocitose
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Murine-Derived); 0 (Antigens, CD); 0 (Antigens, CD20); 0 (Antigens, Neoplasm); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Epitopes); 0 (Glycoproteins); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601473


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[PMID]:28363905
[Au] Autor:Forsberg MH; Ciecko AE; Bednar KJ; Itoh A; Kachapati K; Ridgway WM; Chen YG
[Ad] Endereço:Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, WI 53226.
[Ti] Título:CD137 Plays Both Pathogenic and Protective Roles in Type 1 Diabetes Development in NOD Mice.
[So] Source:J Immunol;198(10):3857-3868, 2017 May 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported that CD137 (encoded by ) deficiency suppressed type 1 diabetes (T1D) progression in NOD mice. We also demonstrated that soluble CD137 produced by regulatory T cells contributed to their autoimmune-suppressive function in this model. These results suggest that CD137 can either promote or suppress T1D development in NOD mice depending on where it is expressed. In this study, we show that NOD. CD8 T cells had significantly reduced diabetogenic capacity, whereas absence of CD137 in non-T and non-B cells had a limited impact on T1D progression. In contrast, NOD. CD4 T cells highly promoted T1D development. We further demonstrated that CD137 was important for the accumulation of ß cell-autoreactive CD8 T cells but was dispensable for their activation in pancreatic lymph nodes. The frequency of islet-infiltrating CD8 T cells was reduced in NOD. mice in part because of their decreased proliferation. Furthermore, CD137 deficiency did not suppress T1D development in NOD mice expressing the transgenic NY8.3 CD8 TCR. This suggests that increased precursor frequency of ß cell-autoreactive CD8 T cells in NY8.3 mice obviated a role for CD137 in diabetogenesis. Finally, blocking CD137-CD137 ligand interaction significantly delayed T1D onset in NOD mice. Collectively, our results indicate that one important diabetogenic function of CD137 is to promote the expansion and accumulation of ß cell-autoreactive CD8 T cells, and in the absence of CD137 or its interaction with CD137 ligand, T1D progression is suppressed.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/imunologia
Diabetes Mellitus Tipo 1/fisiopatologia
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Ligante 4-1BB/antagonistas & inibidores
Ligante 4-1BB/metabolismo
Animais
Linfócitos T CD8-Positivos/imunologia
Proliferação Celular
Progressão da Doença
Células Secretoras de Insulina/imunologia
Camundongos
Camundongos Endogâmicos NOD
Camundongos Transgênicos
Linfócitos T Reguladores/imunologia
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/deficiência
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-1BB Ligand); 0 (Tnfsf9 protein, mouse); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170402
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601851


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[PMID]:28360282
[Au] Autor:Clouthier DL; Ohashi PS
[Ad] Endereço:Princess Margaret Cancer Centre, Campbell Family Institute for Breast Cancer Research, Toronto, ON, Canada.
[Ti] Título:Costimulation, a surprising connection for immunotherapy.
[So] Source:Science;355(6332):1373-1374, 2017 03 31.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Imunoterapia
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral
[Mh] Termos MeSH secundário: Antígenos CD28
Seres Humanos
Ativação Linfocitária
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (CD28 Antigens); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170401
[St] Status:MEDLINE
[do] DOI:10.1126/science.aan1467


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[PMID]:28347235
[Au] Autor:Bagheri S; Yousefi M; Safaie Qamsari E; Riazi-Rad F; Abolhassani M; Younesi V; Dorostkar R; Movassaghpour AA; Sharifzadeh Z
[Ad] Endereço:1 Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
[Ti] Título:Selection of single chain antibody fragments binding to the extracellular domain of 4-1BB receptor by phage display technology.
[So] Source:Tumour Biol;39(3):1010428317695924, 2017 Mar.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The 4-1BB is a surface glycoprotein that pertains to the tumor necrosis factor-receptor family. There is compelling evidence suggesting important roles for 4-1BB in the immune response, including cell activation and proliferation and also cytokine induction. Because of encouraging results of different agonistic monoclonal antibodies against 4-1BB in the treatment of cancer, infectious, and autoimmune diseases, 4-1BB has been suggested as an attractive target for immunotherapy. In this study, single chain variable fragment phage display libraries, Tomlinson I+J, were screened against specific synthetic oligopeptides (peptides I and II) designed from 4-1BB extracellular domain. Five rounds of panning led to selection of four 4-1BB specific single chain variable fragments (PI.12, PI.42, PII.16, and PII.29) which showed specific reaction to relevant peptides in phage enzyme-linked immunosorbent assay. The selected clones were successfully expressed in Escherichia coli Rosetta-gami 2, and their expression was confirmed by western blot analysis. Enzyme-linked immunosorbent assay experiments indicated that these antibodies were able to specifically recognize 4-1BB without any cross-reactivity with other antigens. Flow cytometry analysis demonstrated an acceptable specific binding of the single chain variable fragments to 4-1BB expressed on CCRF-CEM cells, while no binding was observed with an irrelevant antibody. Anti-4-1BB single chain variable fragments enhanced surface CD69 expression and interleukin-2 production in stimulated CCRF-CEM cells which confirmed the agonistic effect of the selected single chain variable fragments. The data from this study have provided a rationale for further experiments involving the biological functions of anti-4-1BB single chain variable fragments in future studies.
[Mh] Termos MeSH primário: Anticorpos Anti-Idiotípicos/imunologia
Imunoterapia
Leucemia/imunologia
Anticorpos de Cadeia Única/imunologia
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Mh] Termos MeSH secundário: Anticorpos Anti-Idiotípicos/uso terapêutico
Antígenos CD/biossíntese
Antígenos de Diferenciação de Linfócitos T/biossíntese
Antígenos de Neoplasias/imunologia
Linhagem Celular Tumoral
Escherichia coli/genética
Citometria de Fluxo
Seres Humanos
Imunidade Inata
Interleucina-2/biossíntese
Lectinas Tipo C/biossíntese
Leucemia/terapia
Biblioteca de Peptídeos
Peptídeos/imunologia
Peptídeos/uso terapêutico
Domínios Proteicos/imunologia
Anticorpos de Cadeia Única/isolamento & purificação
Anticorpos de Cadeia Única/uso terapêutico
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/isolamento & purificação
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Anti-Idiotypic); 0 (Antigens, CD); 0 (Antigens, Differentiation, T-Lymphocyte); 0 (Antigens, Neoplasm); 0 (CD69 antigen); 0 (Interleukin-2); 0 (Lectins, C-Type); 0 (Peptide Library); 0 (Peptides); 0 (Single-Chain Antibodies); 0 (TNFRSF9 protein, human); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 9)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317695924



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