// +author:d aschenbrenner +author:aschenbrenner 
var _ajax_res = {
  hits: 7,

  first: 0,

  results: [

{userid:"sabinebartosch", "articletype":"article","pages":"514-8","author":"C E Zielinski, F Mele, D Aschenbrenner, D Jarrossay, F Ronchi, M Gattorno, S Monticelli, A Lanzavecchia, F Sallusto","year":"2012","title":"Pathogen-induced human TH17 cells produce IFN-gamma or IL-10 and are regulated by IL-1beta","month":"","journal":"Nature","publisher":"","volume":"484","number":"7395","note":"","tags":"2012","booktitle":"","editor":"","abstract":"IL-17-producing CD4+ T helper cells (TH17) have been extensively investigated in mouse models of autoimmunity. However, the requirements for differentiation and the properties of pathogen-induced human TH17 cells remain poorly defined. Using an approach that combines the in vitro priming of naive T cells with the ex vivo analysis of memory T cells, we describe here two types of human TH17 cells with distinct effector function and differentiation requirements. Candida albicans-specific TH17 cells produced IL-17 and IFN-gamma, but no IL-10, whereas Staphylococcus aureus-specific TH17 cells produced IL-17 and could produce IL-10 upon restimulation. IL-6, IL-23 and IL-1beta contributed to TH17 differentiation induced by both pathogens, but IL-1beta was essential in C. albicans-induced TH17 differentiation to counteract the inhibitory activity of IL-12 and to prime IL-17\/IFN-gamma double-producing cells. In addition, IL-1beta inhibited IL-10 production in differentiating and in memory TH17 cells, whereas blockade of IL-1beta in vivo led to increased IL-10 production by memory TH17 cells. We also show that, after restimulation, TH17 cells transiently downregulated IL-17 production through a mechanism that involved IL-2-induced activation of STAT5 and decreased expression of ROR-gammat. Taken together these findings demonstrate that by eliciting different cytokines C. albicans and S. aureus prime TH17 cells that produce either IFN-gamma or IL-10, and identify IL-1beta and IL-2 as pro- and anti-inflammatory regulators of TH17 cells both at priming and in the effector phase.","address":"","school":"","issn":"","doi":"10.1038\/nature10957","isi":"","pubmed":"","key":"Zielinski2012a","howpublished":"http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/22466287","urllink":"http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/22466287","refid":7983,"weight":7983}
,

{userid:"sdingel", "articletype":"article","pages":"514-U139","author":"C E Zielinski, F Mele, D Aschenbrenner, D Jarrossay, F Ronchi, M Gattorno, S Monticelli, A Lanzavecchia, F Sallusto","year":"2012","title":"Pathogen-induced human T(H)17 cells produce IFN-gamma or IL-10 and are regulated by IL-1 beta","month":"","journal":"Nature","publisher":"","volume":"484","number":"7395","note":"931FF ;Times Cited:154 ;Cited References Count:30","tags":"2012,website,Feld Z, intern","booktitle":"","editor":"","abstract":"IL-17-producing CD4(+) T helper cells (T(H)17) have been extensively investigated in mouse models of autoimmunity(1). However, the requirements for differentiation and the properties of pathogen-induced human T(H)17 cells remain poorly defined. Using an approach that combines the in vitro priming of naive T cells with the ex vivo analysis of memory T cells, we describe here two types of human T(H)17 cells with distinct effector function and differentiation requirements. Candida albicans-specific T(H)17 cells produced IL-17 and IFN-gamma, but no IL-10, whereas Staphylococcus aureus-specific T(H)17 cells produced IL-17 and could produce IL-10 upon restimulation. IL-6, IL-23 and IL-1 beta contributed to T(H)17 differentiation induced by both pathogens, but IL-1 beta was essential in C. albicans-induced T(H)17 differentiation to counteract the inhibitory activity of IL-12 and to prime IL-17\/IFN-gamma double-producing cells. In addition, IL-1 beta inhibited IL-10 production in differentiating and in memory T(H)17 cells, whereas blockade of IL-1 beta in vivo led to increased IL-10 production by memory T(H)17 cells. We also show that, after restimulation, T(H)17 cells transiently downregulated IL-17 production through a mechanism that involved IL-2-induced activation of STAT5 and decreased expression of ROR-gamma t. Taken together these findings demonstrate that by eliciting different cytokines C. albicans and S. aureus prime T(H)17 cells that produce either IFN-gamma or IL-10, and identify IL-1 beta and IL-2 as pro-and anti-inflammatory regulators of T(H)17 cells both at priming and in the effector phase.","address":"","school":"","issn":"0028-0836","doi":"10.1038\/Nature10957","isi":"","pubmed":"","key":"Zielinski2012a","howpublished":"http:\/\/www.nature.com\/nature\/journal\/v484\/n7395\/full\/nature10957.html","urllink":"http:\/\/www.nature.com\/nature\/journal\/v484\/n7395\/full\/nature10957.html","refid":69058,"weight":69058}
,

{userid:"Sekretariat", "articletype":"article","pages":"514-U139","author":"C E Zielinski, F Mele, D Aschenbrenner, D Jarrossay, F Ronchi, M Gattorno, S Monticelli, A Lanzavecchia, F Sallusto","year":"2012","title":"Pathogen-induced human T(H)17 cells produce IFN-gamma or IL-10 and are regulated by IL-1 beta","month":"","journal":"Nature","publisher":"","volume":"484","number":"7395","note":"931FF xD;Times Cited:154 xD;Cited References Count:30","tags":"2012,website,Feld Z, intern","booktitle":"","editor":"","abstract":"IL-17-producing CD4(+) T helper cells (T(H)17) have been extensively investigated in mouse models of autoimmunity(1). However, the requirements for differentiation and the properties of pathogen-induced human T(H)17 cells remain poorly defined. Using an approach that combines the in vitro priming of naive T cells with the ex vivo analysis of memory T cells, we describe here two types of human T(H)17 cells with distinct effector function and differentiation requirements. Candida albicans-specific T(H)17 cells produced IL-17 and IFN-gamma, but no IL-10, whereas Staphylococcus aureus-specific T(H)17 cells produced IL-17 and could produce IL-10 upon restimulation. IL-6, IL-23 and IL-1 beta contributed to T(H)17 differentiation induced by both pathogens, but IL-1 beta was essential in C. albicans-induced T(H)17 differentiation to counteract the inhibitory activity of IL-12 and to prime IL-17\/IFN-gamma double-producing cells. In addition, IL-1 beta inhibited IL-10 production in differentiating and in memory T(H)17 cells, whereas blockade of IL-1 beta in vivo led to increased IL-10 production by memory T(H)17 cells. We also show that, after restimulation, T(H)17 cells transiently downregulated IL-17 production through a mechanism that involved IL-2-induced activation of STAT5 and decreased expression of ROR-gamma t. Taken together these findings demonstrate that by eliciting different cytokines C. albicans and S. aureus prime T(H)17 cells that produce either IFN-gamma or IL-10, and identify IL-1 beta and IL-2 as pro-and anti-inflammatory regulators of T(H)17 cells both at priming and in the effector phase.","address":"","school":"","issn":"0028-0836","doi":"10.1038\/Nature10957","isi":"","pubmed":"","key":"Zielinski2012a","howpublished":"http:\/\/www.nature.com\/nature\/journal\/v484\/n7395\/full\/nature10957.html","urllink":"http:\/\/www.nature.com\/nature\/journal\/v484\/n7395\/full\/nature10957.html","refid":11830,"weight":11830}
,

{userid:"Sekretariat", "articletype":"article","pages":"514-U139","author":"C E Zielinski, F Mele, D Aschenbrenner, D Jarrossay, F Ronchi, M Gattorno, S Monticelli, A Lanzavecchia, F Sallusto","year":"2012","title":"Pathogen-induced human T(H)17 cells produce IFN-gamma or IL-10 and are regulated by IL-1 beta","month":"","journal":"Nature","publisher":"","volume":"484","number":"7395","note":"931FF xD;Times Cited:154 xD;Cited References Count:30","tags":"2012,website,Feld Z, intern","booktitle":"","editor":"","abstract":"IL-17-producing CD4(+) T helper cells (T(H)17) have been extensively investigated in mouse models of autoimmunity(1). However, the requirements for differentiation and the properties of pathogen-induced human T(H)17 cells remain poorly defined. Using an approach that combines the in vitro priming of naive T cells with the ex vivo analysis of memory T cells, we describe here two types of human T(H)17 cells with distinct effector function and differentiation requirements. Candida albicans-specific T(H)17 cells produced IL-17 and IFN-gamma, but no IL-10, whereas Staphylococcus aureus-specific T(H)17 cells produced IL-17 and could produce IL-10 upon restimulation. IL-6, IL-23 and IL-1 beta contributed to T(H)17 differentiation induced by both pathogens, but IL-1 beta was essential in C. albicans-induced T(H)17 differentiation to counteract the inhibitory activity of IL-12 and to prime IL-17\/IFN-gamma double-producing cells. In addition, IL-1 beta inhibited IL-10 production in differentiating and in memory T(H)17 cells, whereas blockade of IL-1 beta in vivo led to increased IL-10 production by memory T(H)17 cells. We also show that, after restimulation, T(H)17 cells transiently downregulated IL-17 production through a mechanism that involved IL-2-induced activation of STAT5 and decreased expression of ROR-gamma t. Taken together these findings demonstrate that by eliciting different cytokines C. albicans and S. aureus prime T(H)17 cells that produce either IFN-gamma or IL-10, and identify IL-1 beta and IL-2 as pro-and anti-inflammatory regulators of T(H)17 cells both at priming and in the effector phase.","address":"","school":"","issn":"0028-0836","doi":"10.1038\/Nature10957","isi":"","pubmed":"","key":"Zielinski2012a","howpublished":"http:\/\/www.nature.com\/nature\/journal\/v484\/n7395\/full\/nature10957.html","urllink":"http:\/\/www.nature.com\/nature\/journal\/v484\/n7395\/full\/nature10957.html","refid":13608,"weight":13608}
,

{userid:"Sekretariat", "articletype":"article","pages":"514-U139","author":"C E Zielinski, F Mele, D Aschenbrenner, D Jarrossay, F Ronchi, M Gattorno, S Monticelli, A Lanzavecchia, F Sallusto","year":"2012","title":"Pathogen-induced human T(H)17 cells produce IFN-gamma or IL-10 and are regulated by IL-1 beta","month":"","journal":"Nature","publisher":"","volume":"484","number":"7395","note":"931FF  ;Times Cited:154  ;Cited References Count:30","tags":"2012,website,Feld Z, intern","booktitle":"","editor":"","abstract":"IL-17-producing CD4(+) T helper cells (T(H)17) have been extensively investigated in mouse models of autoimmunity(1). However, the requirements for differentiation and the properties of pathogen-induced human T(H)17 cells remain poorly defined. Using an approach that combines the in vitro priming of naive T cells with the ex vivo analysis of memory T cells, we describe here two types of human T(H)17 cells with distinct effector function and differentiation requirements. Candida albicans-specific T(H)17 cells produced IL-17 and IFN-gamma, but no IL-10, whereas Staphylococcus aureus-specific T(H)17 cells produced IL-17 and could produce IL-10 upon restimulation. IL-6, IL-23 and IL-1 beta contributed to T(H)17 differentiation induced by both pathogens, but IL-1 beta was essential in C. albicans-induced T(H)17 differentiation to counteract the inhibitory activity of IL-12 and to prime IL-17\/IFN-gamma double-producing cells. In addition, IL-1 beta inhibited IL-10 production in differentiating and in memory T(H)17 cells, whereas blockade of IL-1 beta in vivo led to increased IL-10 production by memory T(H)17 cells. We also show that, after restimulation, T(H)17 cells transiently downregulated IL-17 production through a mechanism that involved IL-2-induced activation of STAT5 and decreased expression of ROR-gamma t. Taken together these findings demonstrate that by eliciting different cytokines C. albicans and S. aureus prime T(H)17 cells that produce either IFN-gamma or IL-10, and identify IL-1 beta and IL-2 as pro-and anti-inflammatory regulators of T(H)17 cells both at priming and in the effector phase.","address":"","school":"","issn":"0028-0836","doi":"10.1038\/Nature10957","isi":"","pubmed":"","key":"Zielinski2012a","howpublished":"http:\/\/www.nature.com\/nature\/journal\/v484\/n7395\/full\/nature10957.html","urllink":"http:\/\/www.nature.com\/nature\/journal\/v484\/n7395\/full\/nature10957.html","refid":15386,"weight":15386}
,

{userid:"cellular.neurology", "refid":"391","repocollections":"","attachment":"","_thumb":"","articletype":"article","sectionheading":"","title":"Downstream Biomarker Effects of Gantenerumab or Solanezumab in Dominantly Inherited Alzheimer Disease: The DIAN-TU-001 Randomized Clinical Trial.","year":"2024","author":"Olivia Wagemann, Haiyan Liu, Guoqiao Wang, Xinyu Shi, Tobias Bittner, Marzia A Scelsi, Martin R Farlow, David B Clifford, Charlene Supnet-Bell, Anna M Santacruz, Andrew J Aschenbrenner, Jason J Hassenstab, Tammie L S Benzinger, Brian A Gordon, Kelley A Coalier, Carlos Cruchaga, Laura Ibanez, Richard J Perrin, Chengjie Xiong, Yan Li, John C Morris, James J Lah, Sarah B Berman, Erik D Roberson, Christopher H van Dyck, Douglas Galasko, Serge Gauthier, Ging-Yuek R Hsiung, William S Brooks, J\u00e9r\u00e9mie Pariente, Catherine J Mummery, Gregory S Day, John M Ringman, Patricio Chrem Mendez, Peter St George-Hyslop, Nick C Fox, Kazushi Suzuki, Hamid R Okhravi, Jasmeer Chhatwal, Johannes Levin, Mathias Jucker, John R Sims, Karen C Holdridge, Nicholas K Proctor, Roy Yaari, Scott W Andersen, Michele Mancini, Jorge Llibre-Guerra, Randall J Bateman, Eric McDade,  ","journal":"JAMA neurology","volume":"81","number":"6","pages":"582-593","month":"Jun","doi":"10.1002\/alz.13031","pubmed":"38683602","pdflink":"","urllink":"","abstract":"Effects of antiamyloid agents, targeting either fibrillar or soluble monomeric amyloid peptides, on downstream biomarkers in cerebrospinal fluid (CSF) and plasma are largely unknown in dominantly inherited Alzheimer disease (DIAD).","note":"","tags":"Humans,Antibodies, Monoclonal, Humanized,Female,Male,Alzheimer Disease,Double-Blind Method,Middle Aged,Biomarkers,Adult,Amyloid beta-Peptides,Chitinase-3-Like Protein 1,Aged,Neurofilament Proteins","weight":391,"publisher":"","booktitle":"","editor":"","address":"","school":"","issn":"2168-6157","isi":"","key":"Wagemann2024","howpublished":""}
,

{userid:"cellular.neurology", "refid":"325","repocollections":"","attachment":"","_thumb":"","articletype":"article","sectionheading":"","title":"Longitudinal clinical, cognitive and biomarker profiles in dominantly inherited versus sporadic early-onset Alzheimer's disease.","year":"2023","author":"Jorge J Llibre-Guerra, Leonardo Iaccarino, Dean Coble, Lauren Edwards, Yan Li, Eric McDade, Amelia Strom, Brian Gordon, Nidhi Mundada, Suzanne E Schindler, Elena Tsoy, Yinjiao Ma, Ruijin Lu, Anne M Fagan, Tammie L S Benzinger, David Soleimani-Meigooni, Andrew J Aschenbrenner, Zachary Miller, Guoqiao Wang, Joel H Kramer, Jason Hassenstab, Howard J Rosen, John C Morris, Bruce L Miller, Chengjie Xiong, Richard J Perrin, Ricardo Allegri, Patricio Chrem, Ezequiel Surace, Sarah B Berman, Jasmeer Chhatwal, Colin L Masters, Martin R Farlow, Mathias Jucker, Johannes Levin, Nick C Fox, Gregory Day, Maria Luisa Gorno-Tempini, Adam L Boxer, Renaud La Joie, Gil D Rabinovici, Randall Bateman","journal":"Brain communications","volume":"5","number":"6","pages":"","month":"10","doi":"10.1093\/braincomms\/fcad280","pubmed":"37942088","pdflink":"","urllink":"","abstract":"Approximately 5% of Alzheimer's disease cases have an early age at onset (<65 years), with 5-10% of these cases attributed to dominantly inherited mutations and the remainder considered as sporadic. The extent to which dominantly inherited and sporadic early-onset Alzheimer's disease overlap is unknown. In this study, we explored the clinical, cognitive and biomarker profiles of early-onset Alzheimer's disease, focusing on commonalities and distinctions between dominantly inherited and sporadic cases. Our analysis included 117 participants with dominantly inherited Alzheimer's disease enrolled in the Dominantly Inherited Alzheimer Network and 118 individuals with sporadic early-onset Alzheimer's disease enrolled at the University of California San Francisco Alzheimer's Disease Research Center. Baseline differences in clinical and biomarker profiles between both groups were compared using -tests. Differences in the rates of decline were compared using linear mixed-effects models. Individuals with dominantly inherited Alzheimer's disease exhibited an earlier age-at-symptom onset compared with the sporadic group [43.4 (SD \u00b1 8.5) years versus 54.8 (SD \u00b1 5.0) years, respectively,  < 0.001]. Sporadic cases showed a higher frequency of atypical clinical presentations relative to dominantly inherited (56.8% versus 8.5%, respectively) and a higher frequency of APOE-\u03b54 (50.0% versus 28.2%,  = 0.001). Compared with sporadic early onset, motor manifestations were higher in the dominantly inherited cohort [32.5% versus 16.9% at baseline ( = 0.006) and 46.1% versus 25.4% at last visit ( = 0.001)]. At baseline, the sporadic early-onset group performed worse on category fluency ( < 0.001), Trail Making Test Part B ( < 0.001) and digit span ( < 0.001). Longitudinally, both groups demonstrated similar rates of cognitive and functional decline in the early stages. After 10 years from symptom onset, dominantly inherited participants experienced a greater decline as measured by Clinical Dementia Rating Sum of Boxes [3.63 versus 1.82 points ( = 0.035)]. CSF amyloid beta-42 levels were comparable [244 (SD \u00b1 39.3) pg\/ml dominantly inherited versus 296 (SD \u00b1 24.8) pg\/ml sporadic early onset,  = 0.06]. CSF phosphorylated tau at threonine 181 levels were higher in the dominantly inherited Alzheimer's disease cohort (87.3 versus 59.7\u2005pg\/ml,  = 0.005), but no significant differences were found for t-tau levels ( = 0.35). In summary, sporadic and inherited Alzheimer's disease differed in baseline profiles; sporadic early onset is best distinguished from dominantly inherited by later age at onset, high frequency of atypical clinical presentations and worse executive performance at baseline. Despite these differences, shared pathways in longitudinal clinical decline and CSF biomarkers suggest potential common therapeutic targets for both populations, offering valuable insights for future research and clinical trial design.","note":"","tags":"","weight":325,"publisher":"","booktitle":"","editor":"","address":"","school":"","issn":"2632-1297","isi":"","key":"Llibre-Guerra2023","howpublished":""}
  ]
}

;
ajaxResultsLoaded(_ajax_res);