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  1 / 2483 MEDLINE  
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PMID:28458362
Autor:Tanaka K; Yoshitomi T; Hirahara K
Endereço:Biologics & Immuno-Oncology Laboratories, Daiichi Sankyo Co., Ltd.
Título:Elucidation of Distinct Roles of Guinea Pig CXCR1 and CXCR2 in Neutrophil Migration toward IL-8 and GROα by Specific Antibodies.
Fonte:Biol Pharm Bull; 40(5):729-732, 2017.
ISSN:1347-5215
País de publicação:Japan
Idioma:eng
Resumo:Chemokine receptors CXCR1 and CXCR2 are conserved between guinea pigs and humans, but the distinct role of each receptor in chemotactic responses of neutrophils against chemokine ligands has not been elucidated due in part to the lack of specific inhibitors against these receptors in guinea pigs. In this study, we investigated the roles of guinea pig CXCR1 and CXCR2 on neutrophils in chemotactic responses to guinea pig interleukin (IL)-8 and growth-regulated oncogene (GRO)α by using specific inhibitory antibodies against these receptors. Neutrophil migration induced by IL-8 was partially inhibited by either anti-CXCR1 antibody or anti-CXCR2 antibody. In addition, the migration was inhibited completely when both anti-CXCR1 and anti-CXCR2 antibodies were combined. On the other hand, neutrophil migration induced by GROα was not inhibited by anti-CXCR1 antibody while inhibited profoundly by anti-CXCR2 antibody. These results indicated that CXCR1 and CXCR2 mediated migration induced by the IL-8 synergistically and only CXCR2 mediated migration induced by GROα in guinea pig neutrophils. Our findings on ligand selectivity of CXCR1 and CXCR2 in guinea pigs are consistent with those in humans.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antibodies, Blocking); 0 (Chemokine CXCL1); 0 (Interleukin-8); 0 (Receptors, Interleukin-8A); 0 (Receptors, Interleukin-8B)


  2 / 2483 MEDLINE  
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PMID:28468826
Autor:Kerros C; Tripathi SC; Zha D; Mehrens JM; Sergeeva A; Philips AV; Qiao N; Peters HL; Katayama H; Sukhumalchandra P; Ruisaard KE; Perakis AA; St John LS; Lu S; Mittendorf EA; Clise-Dwyer K; Herrmann AC; Alatrash G; Toniatti C; Hanash SM; Ma Q; Molldrem JJ
Endereço:From the University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030.
Título:Neuropilin-1 mediates neutrophil elastase uptake and cross-presentation in breast cancer cells.
Fonte:J Biol Chem; 292(24):10295-10305, 2017 06 16.
ISSN:1083-351X
País de publicação:United States
Idioma:eng
Resumo:Neutrophil elastase (NE) can be rapidly taken up by tumor cells that lack endogenous NE expression, including breast cancer, which results in cross-presentation of PR1, an NE-derived HLA-A2-restricted peptide that is an immunotherapy target in hematological and solid tumor malignancies. The mechanism of NE uptake, however, remains unknown. Using the mass spectrometry-based approach, we identify neuropilin-1 (NRP1) as a NE receptor that mediates uptake and PR1 cross-presentation in breast cancer cells. We demonstrated that soluble NE is a specific, high-affinity ligand for NRP1 with a calculated of 38.7 nm Furthermore, we showed that NRP1 binds to the RR R motif in NE. Notably, NRP1 knockdown with interfering RNA or CRISPR-cas9 system and blocking using anti-NRP1 antibody decreased NE uptake and, subsequently, susceptibility to lysis by PR1-specific cytotoxic T cells. Expression of NRP1 in NRP1-deficient cells was sufficient to induce NE uptake. Altogether, because NRP1 is broadly expressed in tumors, our findings suggest a role for this receptor in immunotherapy strategies that target cross-presented antigens.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
Nome de substância:0 (Antibodies, Blocking); 0 (Ligands); 0 (Neoplasm Proteins); 0 (Peptide Fragments); 0 (Recombinant Proteins); 144713-63-3 (Neuropilin-1); EC 3.4.21.37 (Leukocyte Elastase)


  3 / 2483 MEDLINE  
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PMID:28468886
Autor:Sharma S; Carlsson B; Czakó R; Vene S; Haglund M; Ludvigsson J; Larson G; Hammarström L; Sosnovtsev SV; Atmar RL; Green KY; Estes MK; Svensson L
Endereço:Division of Molecular Virology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Título:Human Sera Collected between 1979 and 2010 Possess Blocking-Antibody Titers to Pandemic GII.4 Noroviruses Isolated over Three Decades.
Fonte:J Virol; 91(14), 2017 Jul 15.
ISSN:1098-5514
País de publicação:United States
Idioma:eng
Resumo:The emergence of pandemic GII.4 norovirus (NoV) strains has been proposed to occur due to changes in receptor usage and thereby to lead to immune evasion. To address this hypothesis, we measured the ability of human sera collected between 1979 and 2010 to block glycan binding of four pandemic GII.4 noroviruses isolated in the last 4 decades. In total, 268 sera were investigated for 50% blocking titer (BT ) values of virus-like particles (VLPs) against pig gastric mucin (PGM) using 4 VLPs that represent different GII.4 norovirus variants identified between 1987 and 2012. Pre- and postpandemic sera (sera collected before and after isolation of the reference NoV strain) efficiently prevented binding of VLP strains MD145 (1987), Grimsby (1995), and Houston (2002), but not the Sydney (2012) strain, to PGM. No statistically significant difference in virus-blocking titers was observed between pre- and postpandemic sera. Moreover, paired sera showed that blocking titers of ≥160 were maintained over a 6-year period against MD145, Grimsby, and Houston VLPs. Significantly higher serum blocking titers (geometric mean titer [GMT], 1,704) were found among IgA-deficient individuals than among healthy blood donors (GMT, 90.9) ( < 0.0001). The observation that prepandemic sera possess robust blocking capacity for viruses identified decades later suggests a common attachment factor, at least until 2002. Our results indicate that serum IgG possesses antibody-blocking capacity and that blocking titers can be maintained for at least 6 years against 3 decades of pandemic GII.4 NoV. Human noroviruses (NoVs) are the major cause of acute gastroenteritis worldwide. Histo-blood group antigens (HBGAs) in saliva and gut recognize NoV and are the proposed ligands that facilitate infection. Polymorphisms in HBGA genes, and in particular a nonsense mutation in (G428A), result in resistance to global dominating GII.4 NoV. The emergence of new pandemic GII.4 strains occurs at intervals of several years and is proposed to be attributable to epochal evolution, including amino acid changes and immune evasion. However, it remains unclear whether exposure to a previous pandemic strain stimulates immunity to a pandemic strain identified decades later. We found that prepandemic sera possess robust virus-blocking capacity against viruses identified several decades later. We also show that serum lacking IgA antibodies is sufficient to block NoV VLP binding to HBGAs. This is essential, considering that 1 in every 600 Caucasian children is IgA deficient.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antibodies, Blocking); 0 (Mucins)


  4 / 2483 MEDLINE  
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PMID:28741316
Autor:Hogg A; Sui Y; Ben-Sasson SZ; Paul WE; Berzofsky JA
Endereço:Vaccine Branch, Center for Cancer Research, National Cancer Institute.
Título:Role of CD4 T cell helper subsets in immune response and deviation of CD8 T cells in mice.
Fonte:Eur J Immunol; 47(12):2059-2069, 2017 Dec.
ISSN:1521-4141
País de publicação:Germany
Idioma:eng
Resumo:The ability of different CD4 T cell subsets to help CD8 T-cell response is not fully understood. Here, we found using the murine system that Th17 cells induced by IL-1ß, unlike Th1, were not effective helpers for antiviral CD8 responses as measured by IFNγ-producing cells or protection against virus infection. However, they skewed CD8 responses to a Tc17 phenotype. Thus, the apparent lack of help was actually immune deviation. This skewing depended on both IL-21 and IL-23. To overcome this effect, we inhibited Th17 induction by blocking TGF-ß. Anti-TGF-ß allowed the IL-1ß adjuvant to enhance CD8 T-cell responses without skewing the phenotype to Tc17, thereby providing an approach to harness the benefit of common IL-1-inducing adjuvants like alum without immune deviation.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antibodies, Blocking); 0 (Epitopes, T-Lymphocyte); 0 (Interleukin-1beta); 0 (Transforming Growth Factor beta); 82115-62-6 (Interferon-gamma)


  5 / 2483 MEDLINE  
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PMID:28979997
Autor:Crespo-Garcia S; Corkhill C; Roubeix C; Davids AM; Kociok N; Strauss O; Joussen AM; Reichhart N
Título:Inhibition of Placenta Growth Factor Reduces Subretinal Mononuclear Phagocyte Accumulation in Choroidal Neovascularization.
Fonte:Invest Ophthalmol Vis Sci; 58(12):4997-5006, 2017 Oct 01.
ISSN:1552-5783
País de publicação:United States
Idioma:eng
Resumo:Purpose: The cellular immune response driven by mononuclear phagocytes (MPs) is crucial for choroidal neovascularization (CNV) progression. Case reports show that a switch from pure anti-vascular endothelial growth factor-A (VEGF-A) intravitreal treatment to aflibercept, a drug with combined anti-VEGF-A and anti-placenta growth factor (PlGF) activity, can be beneficial for patients who do not respond to anti-VEGF-A alone. Since MPs harbor VEGFR1, we hypothesize that the interplay of P1GF/vascular endothelial growth factor receptor 1 (VEGFR1) in immune cells plays a pivotal role for CNV. Methods: CNV was induced with laser, and immune cells and neovascularization were analyzed in vivo and ex vivo. Immunohistochemistry was employed for protein detection. Differential expression of angiogenic factors and macrophage polarization markers were assessed by quantitative PCR (qPCR). One day after laser, intravitreal injection of aflibercept or anti-PlGF was performed. Results: In the early inflammatory phase after laser, Plgf but not Vegfa was significantly upregulated. VEGF-A upregulation is limited to the scar, whereas PlGF shows a wider distribution. M1 (proinflammatory) macrophage markers were upregulated in the early phase of CNV. However, M2 (proangiogenic) markers showed more inconsistent dynamics. We demonstrated that both aflibercept and anti-PlGF treatments decrease the overall amount of activated subretinal MPs, and especially of those expressing PlGF. These data correlated with a reduction in leakage associated to CNV. Aflibercept showed a stronger reduction in both parameters. Conclusions: The results hint at an interplay between PlGF/VEGFR1 and MPs that is important in the early phase of CNV. A combined inhibition of VEGF-A and PlGF is superior to a specific anti-PlGF treatment in terms of subretinal MP recruitment.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Aif1 protein, mouse); 0 (Angiogenesis Inhibitors); 0 (Antibodies, Blocking); 0 (Calcium-Binding Proteins); 0 (Immunologic Factors); 0 (Microfilament Proteins); 0 (Pgf protein, mouse); 0 (Recombinant Fusion Proteins); 0 (Vascular Endothelial Growth Factor A); 0 (vascular endothelial growth factor A, mouse); 144589-93-5 (Placenta Growth Factor); 15C2VL427D (aflibercept); EC 2.7.10.1 (Flt1 protein, mouse); EC 2.7.10.1 (Receptors, Vascular Endothelial Growth Factor); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1)


  6 / 2483 MEDLINE  
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PMID:28904129
Autor:Radomir L; Cohen S; Kramer MP; Bakos E; Lewinsky H; Barak A; Porat Z; Bucala R; Stepensky P; Becker-Herman S; Shachar I
Endereço:Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel.
Título:T Cells Regulate Peripheral Naive Mature B Cell Survival by Cell-Cell Contact Mediated through SLAMF6 and SAP.
Fonte:J Immunol; 199(8):2745-2757, 2017 Oct 15.
ISSN:1550-6606
País de publicação:United States
Idioma:eng
Resumo:The control of lymphoid homeostasis is the result of a very fine balance between lymphocyte production, proliferation, and apoptosis. In this study, we focused on the role of T cells in the maintenance/survival of the mature naive peripheral B cell population. We show that naive B and T cells interact via the signaling lymphocyte activation molecule (SLAM) family receptor, SLAMF6. This interaction induces cell type-specific signals in both cell types, mediated by the SLAM-associated protein (SAP) family of adaptors. This signaling results in an upregulation of the expression of the cytokine migration inhibitory factor in the T cells and augmented expression of its receptor CD74 on the B cell counterparts, consequently enhancing B cell survival. Furthermore, in X-linked lymphoproliferative disease patients, SAP deficiency reduces CD74 expression, resulting in the perturbation of B cell maintenance from the naive stage. Thus, naive T cells regulate B cell survival in a SLAMF6- and SAP-dependent manner.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antibodies, Blocking); 0 (RNA, Small Interfering); 0 (Signaling Lymphocytic Activation Molecule Associated Protein); 0 (Signaling Lymphocytic Activation Molecule Family); 0 (Slamf6 protein, mouse)


  7 / 2483 MEDLINE  
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PMID:28880903
Autor:Goods BA; Hernandez AL; Lowther DE; Lucca LE; Lerner BA; Gunel M; Raddassi K; Coric V; Hafler DA; Love JC
Endereço:Departments of Biological Engineering and Chemical Engineering, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.
Título:Functional differences between PD-1+ and PD-1- CD4+ effector T cells in healthy donors and patients with glioblastoma multiforme.
Fonte:PLoS One; 12(9):e0181538, 2017.
ISSN:1932-6203
País de publicação:United States
Idioma:eng
Resumo:Immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) have been highly successful in the treatment of cancer. While PD-1 expression has been widely investigated, its role in CD4+ effector T cells in the setting of health and cancer remains unclear, particularly in the setting of glioblastoma multiforme (GBM), the most aggressive and common form of brain cancer. We examined the functional and molecular features of PD-1+CD4+CD25-CD127+Foxp3-effector cells in healthy subjects and in patients with GBM. In healthy subjects, we found that PD-1+CD4+ effector cells are dysfunctional: they do not proliferate but can secrete large quantities of IFNγ. Strikingly, blocking antibodies against PD-1 did not rescue proliferation. RNA-sequencing revealed features of exhaustion in PD-1+ CD4 effectors. In the context of GBM, tumors were enriched in PD-1+ CD4+ effectors that were similarly dysfunctional and unable to proliferate. Furthermore, we found enrichment of PD-1+TIM-3+ CD4+ effectors in tumors, suggesting that co-blockade of PD-1 and TIM-3 in GBM may be therapeutically beneficial. RNA-sequencing of blood and tumors from GBM patients revealed distinct differences between CD4+ effectors from both compartments with enrichment in multiple gene sets from tumor infiltrating PD-1-CD4+ effectors cells. Enrichment of these gene sets in tumor suggests a more metabolically active cell state with signaling through other co-receptors. PD-1 expression on CD4 cells identifies a dysfunctional subset refractory to rescue with PD-1 blocking antibodies, suggesting that the influence of immune checkpoint inhibitors may involve recovery of function in the PD-1-CD4+ T cell compartment. Additionally, co-blockade of PD-1 and TIM-3 in GBM may be therapeutically beneficial.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antibodies, Blocking); 0 (Hepatitis A Virus Cellular Receptor 2); 0 (Interleukin-2); 0 (Programmed Cell Death 1 Receptor); 82115-62-6 (Interferon-gamma)


  8 / 2483 MEDLINE  
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PMID:28877988
Autor:Geha M; Tsokos MG; Bosse RE; Sannikova T; Iwakura Y; Dalle Lucca JJ; De Waal Malefyt R; Tsokos GC
Endereço:Department of Pediatrics, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.
Título:IL-17A Produced by Innate Lymphoid Cells Is Essential for Intestinal Ischemia-Reperfusion Injury.
Fonte:J Immunol; 199(8):2921-2929, 2017 Oct 15.
ISSN:1550-6606
País de publicação:United States
Idioma:eng
Resumo:Ischemia-reperfusion (IR) injury to the small intestine following clamping of the superior mesenteric artery results in an intense local inflammatory response that is characterized by villous damage and neutrophil infiltration. IL-17A, a cytokine produced by a variety of cells in response to inflammatory cytokines released following tissue injury, has been implicated in IR injury. Using , , and mice and administration of anti-IL-17A and anti-IL-23 neutralizing Abs to wild-type mice, we demonstrate that intestinal IR injury depends on IL-17A and that IL-17A is downstream of the binding of autoantibody to ischemia-conditioned tissues and subsequent complement activation. Using bone marrow chimeras, we demonstrate that the IL-17A required for intestinal IR injury is derived from hematopoietic cells. Finally, by transferring autoantibody-rich sera into and mice, we demonstrate that innate lymphoid cells are the main producers of IL-17A in intestinal IR injury. We propose that local production of IL-17A by innate lymphoid cells is crucial for the development of intestinal IR injury and may provide a therapeutic target for clinical exploitation.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antibodies, Blocking); 0 (Autoantibodies); 0 (DNA-Binding Proteins); 0 (Interleukin-17); 0 (Nuclear Receptor Subfamily 1, Group F, Member 3); 0 (Rag2 protein, mouse); 0 (Receptors, Interleukin); 0 (Rorc protein, mouse); 0 (interleukin-23 receptor, mouse)


  9 / 2483 MEDLINE  
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PMID:28801234
Autor:Xu MM; Pu Y; Han D; Shi Y; Cao X; Liang H; Chen X; Li XD; Deng L; Chen ZJ; Weichselbaum RR; Fu YX
Endereço:Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75235, USA; Department of Radiation and Cellular Oncology, The Ludwig Center for Metastasis Research, University of Chicago, Chicago, IL 60637, USA.
Título:Dendritic Cells but Not Macrophages Sense Tumor Mitochondrial DNA for Cross-priming through Signal Regulatory Protein α Signaling.
Fonte:Immunity; 47(2):363-373.e5, 2017 Aug 15.
ISSN:1097-4180
País de publicação:United States
Idioma:eng
Resumo:Inhibition of cytosolic DNA sensing represents a strategy that tumor cells use for immune evasion, but the underlying mechanisms are unclear. Here we have shown that CD47-signal regulatory protein α (SIRPα) axis dictates the fate of ingested DNA in DCs for immune evasion. Although macrophages were more potent in uptaking tumor DNA, increase of DNA sensing by blocking the interaction of SIRPα with CD47 preferentially occurred in dendritic cells (DCs) but not in macrophages. Mechanistically, CD47 blockade enabled the activation of NADPH oxidase NOX2 in DCs, which in turn inhibited phagosomal acidification and reduced the degradation of tumor mitochondrial DNA (mtDNA) in DCs. mtDNA was recognized by cyclic-GMP-AMP synthase (cGAS) in the DC cytosol, contributing to type I interferon (IFN) production and antitumor adaptive immunity. Thus, our findings have demonstrated how tumor cells inhibit innate sensing in DCs and suggested that the CD47-SIRPα axis is critical for DC-driven antitumor immunity.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antibodies, Blocking); 0 (Antigens, Differentiation); 0 (CD47 Antigen); 0 (DNA, Mitochondrial); 0 (Interferon Type I); 0 (MPYS protein, mouse); 0 (Membrane Glycoproteins); 0 (Membrane Proteins); 0 (Ptpns1 protein, mouse); 0 (Receptors, Immunologic); 0 (SIRPA protein, human); EC 1.6.3.- (CYBB protein, human); EC 1.6.3.- (NADPH Oxidase 2); EC 1.6.3.- (NADPH Oxidases); EC 2.7.7.- (MB21D1 protein, mouse); EC 2.7.7.- (Nucleotidyltransferases)


  10 / 2483 MEDLINE  
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PMID:28771632
Autor:Shewell LK; Jen FE; Jennings MP
Endereço:Institute for Glycomics, Griffith University, Gold Coast, Queensland, Australia.
Título:Refinement of immunizing antigens to produce functional blocking antibodies against the AniA nitrite reductase of Neisseria gonorrhoeae.
Fonte:PLoS One; 12(8):e0182555, 2017.
ISSN:1932-6203
País de publicação:United States
Idioma:eng
Resumo:The emergence of multi-drug resistant Neisseria gonorrhoeae has generated an urgent need for novel therapies or a vaccine to prevent gonococcal disease. In this study we investigate the potential of targeting the surface exposed nitrite reductase, AniA, to block activity by producing functional blocking antibodies. AniA activity is essential for anaerobic growth and biofilm formation of N. gonorrhoeae and functional blocking antibodies may prevent colonisation and disease. Seven peptides covering regions adjacent to the active site were designed based on the AniA structure. Six of the seven peptide conjugates generated immune responses. Peptide 7, GALGQLKVEGAEN, was able to elicit antibodies capable of blocking AniA activity. Antiserum raised against the peptide 7 conjugate detected AniA in 20 N. gonorrhoeae clinical isolates. Recombinant AniA protein antigens were also assessed in this study and generated high-titre, functional blocking antibody responses. Peptide 7 conjugates or truncated recombinant AniA antigens have potential for inclusion in a vaccine against N. gonorrhoeae.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antibodies, Blocking); 0 (Antigens, Bacterial); 0 (Bacterial Outer Membrane Proteins); 0 (Bacterial Vaccines); 0 (Peptides); 0 (Recombinant Proteins); 0 (aniA protein, Neisseria gonorrhoeae)



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