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[PMID]:29284783
[Au] Autor:Gordiienko I; Shlapatska L; Kholodniuk VM; Kovalevska L; Ivanivskaya TS; Sidorenko SP
[Ad] Endereço:Department of Molecular and Cellular Pathobiology, R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology, NAS of Ukraine, Kyiv 03022, Ukraine.
[Ti] Título:CD150 and CD180 are involved in regulation of transcription factors expression in chronic lymphocytic leukemia cells.
[So] Source:Exp Oncol;39(4):291-298, 2017 Dec.
[Is] ISSN:1812-9269
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sequential stages of B-cell development is stringently coordinated by transcription factors (TFs) network that include B-lineage commitment TFs (Ikaros, Runx1/Cbfb, E2A, and FOXO1), B-lineage maintenance TFs (EBF1 and PAX5) and stage specific set of TFs (IRF4, IRF8, BCL6, BLIMP1). Deregulation of TFs expression and activity is often occurs in malignant B cells. The aim of this study was to evaluate TFs expression in chronic lymphocytic leukemia cells taking into consideration CD150 cell surface expression. From other side we attempted to regulate TFs expression via CD150 and CD180 cell surface receptors. MATERIALS AND METHODS: Studies were performed on normal peripheral blood B-cell subpopulations and chronic lymphocytic leukemia (CLL) cells isolated from peripheral blood of 67 primary untreated patients with CLL. Evaluation of TFs expression was performed on mRNA level using qRT-PCR and on protein level by western blot analysis. RESULTS: Median of PAX5 and EBF1 mRNA expression was higher in cell surface CD150 positive (csCD150 ) compared to csCD150 CLL cases or normal CD19 and CD19 CD5 B-cell subsets. Differences in mRNA expression of IRF8, IRF4 and BLIMP1 between studied groups of CLL and normal B cells were not revealed. All CLL cases were characterized by downregulated expression of PU.1 and BCL6 mRNAs in comparison to normal B cells. At the same time elevated SPIB mRNA expression level was restricted to CLL cells. Protein expression of IRF4, IRF8 and BCL6 was uniformly distributed between csCD150 and csCD150 CLL cases. PU.1 protein and CD20 that is direct PU.1 target gene positively correlated with CD150 cell surface expression on CLL cells. Ligation of CD150 and CD180 alone or in combination upregulated IRF8 and PU.1 while downregulated the IRF4 mRNA expression. Signaling via CD150 or CD180 alone elevated the level of BCL6 mRNA. Strong downregulation of IRF4 mRNA was observed after CD150, CD180 or CD150 andCD180 coligation on CLL cells. We found that in CLL cells CD150 is a negative regulator of SPIB while CD180 is involved in upregulation of EBF1 expression level. Moreover, CD180 ligation on CLL cells caused increase of CD150 mRNA level that is a one of the EBF1 target genes. CONCLUSIONS: Analysis of TFs expression profile revealed upregulated SPIB mRNA level and downregulated PU.1 in CLL cells. CD150 and CD180 receptors may modulate transcriptional program in CLL cells by regulating the TFs expression levels.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Regulação Neoplásica da Expressão Gênica/fisiologia
Leucemia Linfocítica Crônica de Células B/metabolismo
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
Fatores de Transcrição/biossíntese
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD180 protein, human); 0 (SLAMF1 protein, human); 0 (Transcription Factors); 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE


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[PMID]:28982149
[Au] Autor:Gordiienko I; Shlapatska L; Kholodniuk V; Sklyarenko L; Gluzman DF; Clark EA; Sidorenko SP
[Ad] Endereço:Department of Molecular and Cellular Pathobiology, R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology National Academy of Sciences of Ukraine, Kyiv, Ukraine.
[Ti] Título:The interplay of CD150 and CD180 receptor pathways contribute to the pathobiology of chronic lymphocytic leukemia B cells by selective inhibition of Akt and MAPK signaling.
[So] Source:PLoS One;12(10):e0185940, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell surface expression of CD150 and CD180 receptors in chronic lymphocytic leukemia (CLL) associates with mutational IGHV status and favourable prognosis. Here we show a direct correlation between cell surface expression and colocalization of these receptors on CLL B cells. In the absence of CD150 and CD180 on the cell surface both receptors were expressed in the cytoplasm. The CD150 receptor was colocalized with markers of the endoplasmic reticulum, the Golgi apparatus and early endosomes. In contrast, CD180 was detected preferentially in early endosomes. Analysis of CD150 isoforms differential expression revealed that regardless of CD150 cell surface expression the mCD150 isoform with two ITSM signaling motifs was a predominant CD150 isoform in CLL B cells. The majority of CLL cases had significantly elevated expression level of the soluble sCD150, moreover CLL B cells secrete this isoform. CD150 or CD180 crosslinking on CLL B cells alone led to activation of Akt, mTORC1, ERK1/2, p38MAPK and JNK1/2 networks. Both CD150 and CD180 target the translation machinery through mTOR independent as well as mTOR dependent pathways. Moreover, both these receptors transmit pro-survival signals via Akt-mediated inhibition of GSK3ß and FOXO1/FOXO3a. Unexpectedly, coligation CD150 and CD180 receptors on CLL B cells led to mutual inhibition of the Akt and MAPK pathways. While CD150 and CD180 coligation resulted in reduced phosphorylation of Akt, ERK1/2, c-Jun, RSK, p70S6K, S6RP, and 4E-BP; it led to complete blocking of mTOR and p38MAPK phosphorylation. At the same time coligation of CD150 and CD40 receptors did not result in Akt and MAPK inhibition. This suggests that combination of signals via CD150 and CD180 leads to blocking of pro-survival pathways that may be a restraining factor for neoplastic CLL B cells propagation in more than 50% of CLL cases where these receptors are coexpressed.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Linfócitos B/metabolismo
Leucemia Linfocítica Crônica de Células B/patologia
Sistema de Sinalização das MAP Quinases
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
[Mh] Termos MeSH secundário: Separação Celular
Citometria de Fluxo
Seres Humanos
Leucemia Linfocítica Crônica de Células B/enzimologia
Leucemia Linfocítica Crônica de Células B/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD180 protein, human); 0 (SLAMF1 protein, human); 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185940


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[PMID]:28693884
[Au] Autor:Bispo da Silva A; Cerqueira Coelho PL; Alves Oliveira Amparo J; Alves de Almeida Carneiro MM; Pereira Borges JM; Dos Santos Souza C; Dias Costa MF; Mecha M; Guaza Rodriguez C; Amaral da Silva VD; Lima Costa S
[Ad] Endereço:Laboratory of Neurochemistry and Cell Biology, Department of Biochemistry and Biophysics, Institute of Health Sciences, Federal University of Bahia, 40110-100, Salvador, Bahia, Brazil.
[Ti] Título:The flavonoid rutin modulates microglial/macrophage activation to a CD150/CD206 M2 phenotype.
[So] Source:Chem Biol Interact;274:89-99, 2017 Aug 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Rutin is a glycosylated flavonoid present in many fruits and plants that has been demonstrated to have anti-inflammatory and antioxidant properties. However, little is known about the mechanisms underlying microglial activation and its effects on the regulation of cytokines and chemokines associated with inflammatory responses in the central nervous system. In this study we examined the effect of rutin on resting or lipopolysaccharide (LPS)-stimulated microglia and characterized their modulation to an activated M1 phenotype or an alternatively activated M2 phenotype. Microglial cells were treated with rutin (1-100 µM); alternatively, microglial cells were stimulated with LPS and the cells were then treated with rutin (50 µM). The results revealed that rutin treatment was not toxic to microglial cells and induced a dose-dependent increase in microglial proliferation associated with changes in morphology after 24 h of treatment. Rutin also induced microglial activation characterized by an increase in OX-42 positive cells and a large proportion of cells with a CD150/CD206-positive M2 phenotype. Rutin also induced a decrease in the mRNA levels of TNF, IL1ß, IL6 and iNOS, reduced the production of IL6, TNF, and nitric oxide, and increased production of the M2 regulatory cytokine IL10 and arginase. Rutin also significantly inhibited the LPS-induced expression of PTGS2, IL18 and TGFß mRNA. These findings show that rutin has the ability to promote microglial proliferation and induces microglial polarization to the M2 profile when cells are stimulated with LPS. These results point this flavonoid as a possible alternative in the treatment or prevention of neurodegenerative disorders.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Lectinas Tipo C/metabolismo
Lectinas de Ligação a Manose/metabolismo
Microglia/efeitos dos fármacos
Receptores de Superfície Celular/metabolismo
Rutina/farmacologia
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/química
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Ciclo-Oxigenase 2/metabolismo
Citocinas/análise
Flavonoides/química
Flavonoides/farmacologia
Interleucina-18/genética
Interleucina-18/metabolismo
Lipopolissacarídeos/toxicidade
Ativação de Macrófagos/efeitos dos fármacos
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Microglia/citologia
Microglia/metabolismo
Óxido Nítrico/metabolismo
Fenótipo
Ratos
Ratos Wistar
Rutina/química
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Flavonoids); 0 (Interleukin-18); 0 (Lectins, C-Type); 0 (Lipopolysaccharides); 0 (Mannose-Binding Lectins); 0 (Receptors, Cell Surface); 0 (Transforming Growth Factor beta); 0 (mannose receptor); 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1); 31C4KY9ESH (Nitric Oxide); 5G06TVY3R7 (Rutin); EC 1.14.99.1 (Cyclooxygenase 2)
[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:170712
[St] Status:MEDLINE


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[PMID]:28667750
[Au] Autor:Tornack J; Kawano Y; Garbi N; Hämmerling GJ; Melchers F; Tsuneto M
[Ad] Endereço:Senior Group Lymphocyte Development, Max Planck Institute for Infection Biology, Berlin, Germany.
[Ti] Título:Flt3 ligand-eGFP-reporter expression characterizes functionally distinct subpopulations of CD150 long-term repopulating murine hematopoietic stem cells.
[So] Source:Eur J Immunol;47(9):1477-1487, 2017 Sep.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The pool of hematopoietic stem cells (HSCs) in the bone marrow is a mixture of resting, proliferating, and differentiating cells. Long-term repopulating HSCs (LT-HSC) are routinely enriched as Lin Sca1 c-Kit CD34 Flt3 CD150 CD48 cells. The Flt3 ligand (Flt3L) and its receptor Flt3 are important regulators of HSC maintenance, expansion and differentiation. Using Flt3L-eGFP reporter mice, we show that endogenous Flt3L-eGFP-reporter RNA expression correlates with eGFP-protein expression. This Flt3L-eGFP-reporter expression distinguishes two LT-HSC populations with differences in gene expressions and reconstituting potential. Thus, Flt3L-eGFP-reporter cells are identified as predominantly resting HSCs with long-term repopulating capacities. In contrast, Flt3L-eGFP-reporter cells are in majority proliferating HSCs with only short-term repopulating capacities. Flt3L-eGFP-reporter cells express hypoxia, autophagy-inducing, and the LT-HSC-associated genes HoxB5 and Fgd5, while Flt3L-eGFP-reporter HSCs upregulate genes involved in HSC differentiation. Flt3L-eGFP-reporter cells develop to Flt3L-eGFP-reporter cells in vitro, although Flt3L-eGFP-reporter cells remain Flt3L-eGFP-reporter . CD150 Flt3L-eGFP-reporter cells express either endothelial protein C receptor (EPCR) or CD41, while Flt3L-eGFP-reporter cells do express EPCR but not CD41. Thus, FACS-enrichment of Flt3/ Flt3L-eGFP-reporter negative, Lin CD150 CD48 EPCR CD41 HSCs allows a further 5-fold enrichment of functional LT-HSCs.
[Mh] Termos MeSH primário: Células da Medula Óssea/fisiologia
Células-Tronco Hematopoéticas/fisiologia
Proteínas de Membrana/metabolismo
[Mh] Termos MeSH secundário: Animais
Autofagia/genética
Diferenciação Celular
Proliferação Celular
Autorrenovação Celular
Células Cultivadas
Genes Reporter/genética
Proteínas de Fluorescência Verde/genética
Fatores de Troca do Nucleotídeo Guanina/genética
Fatores de Troca do Nucleotídeo Guanina/metabolismo
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/metabolismo
Hipóxia/genética
Proteínas de Membrana/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FGD5 protein, mouse); 0 (Guanine Nucleotide Exchange Factors); 0 (Homeodomain Proteins); 0 (Hoxb5 protein, mouse); 0 (Membrane Proteins); 0 (flt3 ligand protein); 147336-22-9 (Green Fluorescent Proteins); 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170702
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646730


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[PMID]:28373584
[Au] Autor:Baglaenko Y; Cruz Tleugabulova M; Gracey E; Talaei N; Manion KP; Chang NH; Ferri DM; Mallevaey T; Wither JE
[Ad] Endereço:Krembil Research Institute, University Health Network, Toronto, Ontario M5T 2S8, Canada.
[Ti] Título:Invariant NKT Cell Activation Is Potentiated by Homotypic -Ly108 Interactions.
[So] Source:J Immunol;198(10):3949-3962, 2017 May 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Invariant NKT (iNKT) cells are innate lymphocytes that respond to glycolipids presented by the MHC class Ib molecule CD1d and are rapidly activated to produce large quantities of cytokines and chemokines. iNKT cell development uniquely depends on interactions between double-positive thymocytes that provide key homotypic interactions between signaling lymphocyte activation molecule (SLAM) family members. However, the role of SLAM receptors in the differentiation of iNKT cell effector subsets and activation has not been explored. In this article, we show that C57BL/6 mice containing the New Zealand Black locus have profound alterations in Ly108, CD150, and Ly9 expression that is associated with iNKT cell hyporesponsiveness. This loss of function was only apparent when dendritic cells and iNKT cells had a loss of SLAM receptor expression. Using small interfering RNA knockdowns and peptide-blocking strategies, we demonstrated that -Ly108 interactions between dendritic cells and iNKT cells are critical for robust activation. LY108 costimulation similarly increased human iNKT cell activation. Thus, in addition to its established role in iNKT cell ontogeny, Ly108 regulates iNKT cell function in mice and humans.
[Mh] Termos MeSH primário: Antígenos Ly/metabolismo
Células Dendríticas/metabolismo
Ativação Linfocitária
Células T Matadoras Naturais/imunologia
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos CD1d/imunologia
Antígenos Ly/genética
Antígenos Ly/imunologia
Diferenciação Celular
Citocinas/biossíntese
Citocinas/imunologia
Células Dendríticas/imunologia
Regulação da Expressão Gênica
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Células T Matadoras Naturais/metabolismo
RNA Interferente Pequeno
Família de Moléculas de Sinalização da Ativação Linfocitária/deficiência
Família de Moléculas de Sinalização da Ativação Linfocitária/genética
Família de Moléculas de Sinalização da Ativação Linfocitária/imunologia
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/genética
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD1d); 0 (Antigens, Ly); 0 (Cytokines); 0 (Ly108 protein, mouse); 0 (Ly9 protein, mouse); 0 (RNA, Small Interfering); 0 (SLAMF6 protein, human); 0 (Signaling Lymphocytic Activation Molecule Family); 0 (Slamf1 protein, mouse); 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170405
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601369


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[PMID]:28100610
[Au] Autor:Gonçalves-Carneiro D; McKeating JA; Bailey D
[Ad] Endereço:Centre for Human Virology, Institute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
[Ti] Título:The Measles Virus Receptor SLAMF1 Can Mediate Particle Endocytosis.
[So] Source:J Virol;91(7), 2017 Apr 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The signaling lymphocyte activation molecule F1 (SLAMF1) is both a microbial sensor and entry receptor for measles virus (MeV). Herein, we describe a new role for SLAMF1 to mediate MeV endocytosis that is in contrast with the alternative, and generally accepted, model that MeV genome enters cells only after fusion at the cell surface. We demonstrated that MeV engagement of SLAMF1 induces dramatic but transient morphological changes, most prominently in the formation of membrane blebs, which were shown to colocalize with incoming viral particles, and rearrangement of the actin cytoskeleton in infected cells. MeV infection was dependent on these dynamic cytoskeletal changes as well as fluid uptake through a macropinocytosis-like pathway as chemical inhibition of these processes inhibited entry. Moreover, we identified a role for the RhoA-ROCK-myosin II signaling axis in this MeV internalization process, highlighting a novel role for this recently characterized pathway in virus entry. Our study shows that MeV can hijack a microbial sensor normally involved in bacterial phagocytosis to drive endocytosis using a complex pathway that shares features with canonical viral macropinocytosis, phagocytosis, and mechanotransduction. This uptake pathway is specific to SLAMF1-positive cells and occurs within 60 min of viral attachment. Measles virus remains a significant cause of mortality in human populations, and this research sheds new light on the very first steps of infection of this important pathogen. Measles is a significant disease in humans and is estimated to have killed over 200 million people since records began. According to current World Health Organization statistics, it still kills over 100,000 people a year, mostly children in the developing world. The causative agent, measles virus, is a small enveloped RNA virus that infects a broad range of cells during infection. In particular, immune cells are infected via interactions between glycoproteins found on the surface of the virus and SLAMF1, the immune cell receptor. In this study, we have investigated the steps governing entry of measles virus into SLAMF1-positive cells and identified endocytic uptake of viral particles. This research will impact our understanding of morbillivirus-related immunosuppression as well as the application of measles virus as an oncolytic therapeutic.
[Mh] Termos MeSH primário: Endocitose
Vírus do Sarampo/fisiologia
Sarampo/virologia
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/fisiologia
[Mh] Termos MeSH secundário: Células A549
Caveolinas/metabolismo
Clatrina/metabolismo
Citoesqueleto/ultraestrutura
Citoesqueleto/virologia
Dinaminas/metabolismo
Células HEK293
Seres Humanos
Microdomínios da Membrana/virologia
Transdução de Sinais
Vírion/fisiologia
Ligação Viral
Internalização do Vírus
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caveolins); 0 (Clathrin); 0 (DNM2 protein, human); 0 (SLAMF1 protein, human); 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1); EC 3.6.5.5 (Dynamins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE


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[PMID]:28049627
[Au] Autor:Chen S; Cai C; Li Z; Liu G; Wang Y; Blonska M; Li D; Du J; Lin X; Yang M; Dong Z
[Ad] Endereço:Institute for Immunology and School of Medicine, Tsinghua University, Beijing 100086, China.
[Ti] Título:Dissection of SAP-dependent and SAP-independent SLAM family signaling in NKT cell development and humoral immunity.
[So] Source:J Exp Med;214(2):475-489, 2017 Feb.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Signaling lymphocytic activation molecule (SLAM)-associated protein (SAP) mutations in X-linked lymphoproliferative disease (XLP) lead to defective NKT cell development and impaired humoral immunity. Because of the redundancy of SLAM family receptors (SFRs) and the complexity of SAP actions, how SFRs and SAP mediate these processes remains elusive. Here, we examined NKT cell development and humoral immunity in mice completely deficient in SFR. We found that SFR deficiency severely impaired NKT cell development. In contrast to SAP deficiency, SFR deficiency caused no apparent defect in follicular helper T (T ) cell differentiation. Intriguingly, the deletion of SFRs completely rescued the severe defect in T cell generation caused by SAP deficiency, whereas SFR deletion had a minimal effect on the defective NKT cell development in SAP-deficient mice. These findings suggest that SAP-dependent activating SFR signaling is essential for NKT cell selection; however, SFR signaling is inhibitory in SAP-deficient T cells. Thus, our current study revises our understanding of the mechanisms underlying T cell defects in patients with XLP.
[Mh] Termos MeSH primário: Células T Matadoras Naturais/fisiologia
Transdução de Sinais/fisiologia
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/fisiologia
Família de Moléculas de Sinalização da Ativação Linfocitária/fisiologia
[Mh] Termos MeSH secundário: Animais
Antígenos Ly/fisiologia
Proteínas Adaptadoras de Sinalização CARD/fisiologia
Imunidade Humoral
Fatores de Transcrição Kruppel-Like/biossíntese
Transtornos Linfoproliferativos/genética
Camundongos
Fosfatidilinositol-3,4,5-Trifosfato 5-Fosfatases/fisiologia
Proteína com Dedos de Zinco da Leucemia Promielocítica
Proteína Associada à Molécula de Sinalização da Ativação Linfocitária/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (CARD Signaling Adaptor Proteins); 0 (Card11 protein, mouse); 0 (Kruppel-Like Transcription Factors); 0 (Ly108 protein, mouse); 0 (Promyelocytic Leukemia Zinc Finger Protein); 0 (Signaling Lymphocytic Activation Molecule Associated Protein); 0 (Signaling Lymphocytic Activation Molecule Family); 0 (Slamf1 protein, mouse); 0 (Zbtb16 protein, mouse); 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1); EC 3.1.3.86 (Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases)
[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:170105
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161312


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[PMID]:28046053
[Au] Autor:Tornack J; Reece ST; Bauer WM; Vogelzang A; Bandermann S; Zedler U; Stingl G; Kaufmann SH; Melchers F
[Ad] Endereço:Senior Group on Lymphocyte Development, Max Planck Institute for Infection Biology, Berlin, Germany.
[Ti] Título:Human and Mouse Hematopoietic Stem Cells Are a Depot for Dormant Mycobacterium tuberculosis.
[So] Source:PLoS One;12(1):e0169119, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An estimated third of the world's population is latently infected with Mycobacterium tuberculosis (Mtb), with no clinical signs of tuberculosis (TB), but lifelong risk of reactivation to active disease. The niches of persisting bacteria during latent TB infection remain unclear. We detect Mtb DNA in peripheral blood selectively in long-term repopulating pluripotent hematopoietic stem cells (LT-pHSCs) as well as in mesenchymal stem cells from latently infected human donors. In mice infected with low numbers of Mtb, that do not develop active disease we, again, find LT-pHSCs selectively infected with Mtb. In human and mouse LT-pHSCs Mtb are stressed or dormant, non-replicating bacteria. Intratracheal injection of Mtb-infected human and mouse LT-pHSCs into immune-deficient mice resuscitates Mtb to replicating bacteria within the lung, accompanied by signs of active infection. We conclude that LT-pHSCs, together with MSCs of Mtb-infected humans and mice serve as a hitherto unappreciated quiescent cellular depot for Mtb during latent TB infection.
[Mh] Termos MeSH primário: Células-Tronco Hematopoéticas/microbiologia
Tuberculose Latente/microbiologia
Células Mesenquimais Estromais/microbiologia
Mycobacterium tuberculosis
[Mh] Termos MeSH secundário: Adulto
Animais
Antígenos CD34/metabolismo
Células da Medula Óssea/metabolismo
Separação Celular
Feminino
Citometria de Fluxo
Seres Humanos
Pulmão/microbiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Slamf1 protein, mouse); 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1)
[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:170104
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0169119


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[PMID]:27854550
[Au] Autor:Vitales-Noyola M; Ramos-Levi AM; Serrano-Somavilla A; Martínez-Hernández R; Sampedro-Nuñez M; Di Pasquale C; González-Amaro R; Marazuela M
[Ad] Endereço:Department of Immunology, School of Medicine and.
[Ti] Título:Expression and Function of the Costimulatory Receptor SLAMF1 Is Altered in Lymphocytes From Patients With Autoimmune Thyroiditis.
[So] Source:J Clin Endocrinol Metab;102(2):672-680, 2017 Feb 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Signaling lymphocytic activation molecule family 1 (SLAMF1) is a costimulatory receptor expressed by most immune cells. Its role in autoimmune thyroid disease (AITD) is not well known. Objective: To analyze the expression and function of the costimulatory receptor SLAMF1 in lymphocytes of patients with AITD. Design: Cross-sectional, prospective, single-center study. Setting: Department of Endocrinology, Hospital Universitario de la Princesa, Madrid. Patients: Twenty-eight patients with AITD (17 with Graves disease and 11 with Hashimoto thyroiditis) and 21 controls. Intervention: Multiparametric flow cytometry and immunofluorescence techniques to analyze the expression of SLAMF1 in peripheral blood (n = 28) and thyroid tissue (n = 5) mononuclear cells. Assay of inhibition of cellular proliferation to study the function of SLAMF1 in CD4+CD25+ T regulatory (Treg) cells. Main Outcome Measure: Expression levels and the function of SLAMF1 in lymphocytes in AITD patients and controls. Results: Expression of SLAMF1 was significantly increased in peripheral blood CD4+, T helper 17, and CD19+ B cells from AITD patients. Immunofluorescence microscopy detected the presence of SLAMF1+ lymphocytes in thyroid inflammatory cell infiltrate. Functional studies showed that SLAMF1 engagement in Treg cells increased their suppressive function in healthy controls but not in AITD patients. Conclusions: The altered expression of SLAMF1, as well as its defective function observed in patients with AITD, may have a relevant role in the defective immune-regulatory function observed in this condition.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Doença de Graves/sangue
Doença de Hashimoto/sangue
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
Linfócitos T Reguladores/metabolismo
Células Th17/metabolismo
Glândula Tireoide/metabolismo
[Mh] Termos MeSH secundário: Adulto
Antígenos CD19
Estudos Transversais
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD19); 0 (CD19 molecule, human); 0 (SLAMF1 protein, human); 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161118
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-2322


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[PMID]:27573813
[Au] Autor:Guo H; Cranert SA; Lu Y; Zhong MC; Zhang S; Chen J; Li R; Mahl SE; Wu N; Davidson D; Waggoner SN; Veillette A
[Ad] Endereço:Laboratory of Molecular Oncology, Institut de recherches cliniques de Montréal, Montréal, Québec H2W 1R7, Canada Department of Medicine, McGill University, Montréal, Québec H3G 1Y6, Canada.
[Ti] Título:Deletion of Slam locus in mice reveals inhibitory role of SLAM family in NK cell responses regulated by cytokines and LFA-1.
[So] Source:J Exp Med;213(10):2187-207, 2016 Sep 19.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Signaling lymphocytic activation molecule (SLAM) family receptors (SFRs) can mediate either activating or inhibitory effects during natural killer cell (NK cell) activation. In this study, we addressed the global role, regulation, and mechanism of action of the SLAM family in NK cells by analyzing a mouse lacking the entire ∼400-kilobase Slam locus, which encodes all six SFRs and CD48, the ligand of SFR 2B4. This mouse displayed enhanced NK cell activation responses toward hematopoietic target cells. Analyses of mice lacking individual SFRs showed that the inhibitory function of the Slam locus was due solely to 2B4 and was not influenced positively or negatively by other SFRs. Differences in NK cell responses between recognition of targets expressing or lacking ligands for SFRs were enhanced by IL-12 but suppressed by type I interferon. Cytokines also changed the levels of SLAM-associated protein adaptors, which prevent the inhibitory function of SFRs. The enhanced activation responses of SFR-deficient NK cells were dependent on integrin LFA-1 but not on DNAM-1 or NKG2D. SFR-mediated inhibition prevented the generation of activated forms of LFA-1. Hence, the Slam locus has an overall inhibitory role during NK cell activation that is solely dependent on 2B4. This effect is influenced by cytokines and leads to suppression of LFA-1 activity.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Deleção de Genes
Loci Gênicos
Células Matadoras Naturais/metabolismo
Antígeno-1 Associado à Função Linfocitária/metabolismo
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/genética
[Mh] Termos MeSH secundário: Animais
Citotoxicidade Imunológica
Hematopoese
Seres Humanos
Coriomeningite Linfocítica/imunologia
Coriomeningite Linfocítica/virologia
Vírus da Coriomeningite Linfocítica
Camundongos Endogâmicos C57BL
Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cd244 protein, mouse); 0 (Cytokines); 0 (Lymphocyte Function-Associated Antigen-1); 0 (Signaling Lymphocytic Activation Molecule Family); 0 (Slamf1 protein, mouse); 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160831
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20160552



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