97 research outputs found
Exploitation of Herpesvirus Immune Evasion Strategies to Modify the Immunogenicity of Human Mesenchymal Stem Cell Transplants
- Author
- A Bartholomew
- A Corcione
- A Daga
- A Rehm
- A Uccelli
- A Zdoroveac
- AD Hislop
- AD Lipińska
- AM Rodriguez
- Anabel S. de la Garza-Rodea
- Antoine A. F. de Vries
- AS de la Garza-Rodea
- CC Leong
- CL Hsieh
- D Faustman
- D Horst
- D Koppers-Lalic
- D Koppers-Lalic
- Derya Unutmaz
- Dirk W. van Bekkum
- EF Eppens
- EJ Wiertz
- EJ Wiertz
- EJ Wiertz
- Emmanuel J. H. J. Wiertz
- F Morandi
- F Tögel
- G Chen
- GC Hassink
- GM Spaggiari
- GW Wilkinson
- HE Farrell
- Hester Boersma
- HG Ljunggren
- I Rasmusson
- Ietje van der Velde-van Dijke
- J Loureiro
- J van Tuyn
- J van Tuyn
- J Zhang
- JR Smith
- JS Orange
- K Le Blanc
- K Le Blanc
- K Le Blanc
- K Lee
- K Viswanathan
- L Montoliu
- L Zangi
- M Chopp
- M Compte
- M Di Nicola
- MA Gonçalves
- Marieke C. Verweij
- MF Pittenger
- MT Barel
- MT Barel
- MT Barel
- MT Barel
- MT Vossen
- MZ Dewan
- N Eliopoulos
- N Eliopoulos
- N Kotobuki
- O Ringdén
- P Pakzaban
- PA Sotiropoulou
- R Ramasamy
- R Romieu-Mourez
- Rob C. Hoeben
- RP Machold
- S Gasser
- S Knaän-Shanzer
- S Knaän-Shanzer
- S Li
- S Swift
- Shoshan Knaän-Shanzer
- T Kojaoghlanian
- TB Prigozhina
- TH Hansen
- TJ Radosevich
- TM Coyne
- VK Jain
- WM Duan
- XX Jiang
- Y Wang
- Y Ye
- Z Xia
- Publication venue
- Public Library of Science
- Publication date
- 06/01/2011
- Field of study
BACKGROUND: Mesenchymal stem cells (MSCs) are multipotent cells residing in the connective tissue of many organs and holding great potential for tissue repair. In culture, human MSCs (hMSCs) are capable of extensive proliferation without showing chromosomal aberrations. Large numbers of hMSCs can thus be acquired from small samples of easily obtainable tissues like fat and bone marrow. MSCs can contribute to regeneration indirectly by secretion of cytokines or directly by differentiation into specialized cell types. The latter mechanism requires their long-term acceptance by the recipient. Although MSCs do not elicit immune responses in vitro, animal studies have revealed that allogeneic and xenogeneic MSCs are rejected. METHODOLOGY/PRINCIPAL FINDINGS: We aim to overcome MSC immune rejection through permanent down-regulation of major histocompatibility complex (MHC) class I proteins on the surface of these MHC class II-negative cells through the use of viral immune evasion proteins. Transduction of hMSCs with a retroviral vector encoding the human cytomegalovirus US11 protein resulted in strong inhibition of MHC class I surface expression. When transplanted into immunocompetent mice, persistence of the US11-expressing and HLA-ABC-negative hMSCs at levels resembling those found in immunodeficient (i.e., NOD/SCID) mice could be attained provided that recipients' natural killer (NK) cells were depleted prior to cell transplantation. CONCLUSIONS/SIGNIFICANCE: Our findings demonstrate the potential utility of herpesviral immunoevasins to prevent rejection of xenogeneic MSCs. The observation that down-regulation of MHC class I surface expression renders hMSCs vulnerable to NK cell recognition and cytolysis implies that multiple viral immune evasion proteins are likely required to make hMSCs non-immunogenic and thereby universally transplantable
Signal Peptide-Dependent Inhibition of MHC Class I Heavy Chain Translation by Rhesus Cytomegalovirus
- Author
- A Gruhler
- AJ Davison
- AW Sylwester
- B Park
- BE Gewurz
- Colin J. Powers
- D Tortorella
- D Yu
- DJ McGeoch
- EJ Wiertz
- F Momburg
- FJ van der Wal
- G Bacher
- GC Turner
- GW Wilkinson
- H Hengel
- HF Lodish
- JA Urvater
- Jae U. Jung
- JK Kulski
- JL Garrison
- JP Castillo
- Klaus Früh
- M Andersson
- M Goodman
- M Lopez-Botet
- M Ulbrecht
- M Wagner
- MT Barel
- MT Barel
- N Stern-Ginossar
- NJ Stam
- NT Pande
- P Rivailler
- P Tomasec
- R Atalay
- R Daza-Vamenta
- RF Pass
- RP Machold
- S Ito-Harashima
- S Nottrott
- S Oyadomari
- SB Boppana
- SG Hansen
- TA Cha
- TR Jones
- VR DeFilippis
- W Dunn
- W Song
- WA Loenen
- WL Chang
- WL Chang
- WL Chang
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2008
- Field of study
The US2-11 region of human and rhesus cytomegalovirus encodes a conserved family of glycoproteins that inhibit MHC-I assembly with viral peptides, thus preventing cytotoxic T cell recognition. Since HCMV lacking US2-11 is no longer able to block assembly and transport of MHC-I, we examined whether this is also observed for RhCMV lacking the corresponding region. Unexpectedly, recombinant RhCMV lacking US2-11 was still able to inhibit MHC-I expression in infected fibroblasts, suggesting the presence of an additional MHC-I evasion mechanism. Progressive deletion analysis of RhCMV-specific genomic regions revealed that MHC-I expression is fully restored upon additional deletion of rh178. The protein encoded by this RhCMV-specific open reading frame is anchored in the endoplasmic reticulum membrane. In the presence of rh178, RhCMV prevented MHC-I heavy chain (HC) expression, but did not inhibit mRNA transcription or association of HC mRNA with translating ribosomes. Proteasome inhibitors stabilized a HC degradation intermediate in the absence of rh178, but not in its presence, suggesting that rh178 prevents completion of HC translation. This interference was signal sequence-dependent since replacing the signal peptide with that of CD4 or murine HC rendered human HCs resistant to rh178. We have identified an inhibitor of antigen presentation encoded by rhesus cytomegalovirus unique in both its lack of homology to any other known protein and in its mechanism of action. By preventing signal sequence-dependent HC translocation, rh178 acts prior to US2, US3 and US11 which attack MHC-I proteins after protein synthesis is completed. Rh178 is the first viral protein known to interfere at this step of the MHC-I pathway, thus taking advantage of the conserved nature of HC leader peptides, and represents a new mechanism of translational interference
Expression of stabilized β-catenin in differentiated neurons of transgenic mice does not result in tumor formation
- Author
- A Chenn
- A Imbert
- A Koch
- AM Adesina
- AP McMahon
- C Raffel
- C Wetmore
- CG Eberhart
- CW Lam
- D Barel
- D Fults
- DR Borchelt
- H Hahn
- H Huang
- I Smyth
- J Reifenberger
- JJ Lucas
- JL Jankowsky
- K Miyoshi
- L Zeng
- LV Goodrich
- M Peifer
- M van de Wetering
- MD Taylor
- MD Taylor
- MT Furlong
- N Harada
- P Polakis
- RB Halberg
- RH Zurawel
- RP Dahmen
- RT Moon
- SG Megason
- T Pietsch
- WL Perry 3rd
- Y Wang
- Publication venue
- BioMed Central
- Publication date
- 01/01/2002
- Field of study
BACKGROUND: Medulloblastomas, embryonal tumors arising in the cerebellum, commonly contain mutations that activate Wnt signaling. To determine whether increased Wnt signaling in the adult CNS is sufficient to induce tumor formation, we created transgenic mice expressing either wild-type or activated β-catenin in the brain. METHODS: Wild-type and mutant human β-catenin transgenes were expressed under the control of a murine PrP promoter fragment that drives high level postnatal expression in the CNS. Mutant β-catenin was stabilized by a serine to phenylalanine alteration in codon 37. RESULTS: Expression of the mutant transgene resulted in an approximately two-fold increase in β-catenin protein levels in the cortex and cerebellum of adult animals. Immunohistochemical analysis revealed nuclear β-catenin in hippocampal, cortical and cerebellar neurons of transgenic animals but not in non-transgenic controls. Tail kinking was observed in some transgenic animals, but no CNS malformations or tumors were detected. CONCLUSIONS: No tumors or morphologic alterations were detected in the brains of transgenic mice expressing stabilized β-catenin, suggesting that postnatal Wnt signaling in differentiated neurons may not be sufficient to induce CNS tumorigenesis
Modulation of Human Mesenchymal Stem Cell Immunogenicity through Forced Expression of Human Cytomegalovirus US Proteins
- Author
- A Bacigalupo
- A Corcione
- A Li
- A Lin
- A Nasef
- A Rehm
- AI Caplan
- AJ Nauta
- AJ Nauta
- AJ Poncelet
- AS de la Garza-Rodea
- AT Badillo
- B Rolstad
- BN Lilley
- C Bocelli-Tyndall
- C Götherström
- Christopher D. Porada
- D Tortorella
- DM Camp
- DRE Jones
- E Klyushnenkova
- EJ Colletti
- EJ Colletti
- EM Lee
- Esmail D. Zanjani
- Evan Colletti
- EW Petersdorf
- F Morandi
- F Navarro
- F Togel
- FN Meyers JD
- G Maki
- GD Wu
- GM Spaggiari
- Graça Almeida-Porada
- H Zhang
- HKN Obara
- HL Ploegh
- IA Isakova
- J Chamberlain
- JE Gallant
- JM Fletcher
- JY Kim
- K Le Blanc
- K Le Blanc
- K Le Blanc
- KJ Livak
- LL Lanier
- M Di Nicola
- M Mammolenti
- Mariana G. Bego
- MD de Jong
- MD Griffin
- Melisa A. Soland
- MT Barel
- MT Barel
- Mário A. Barbosa
- N Eliopoulos
- N Rouas-Freiss
- PA Sotiropoulou
- PJ Lehner
- PJ Lehner
- R Ramasamy
- R Romieu-Mourez
- RH Lee
- RR Brutkiewicz
- S Bilgrami
- S Jones
- SH Yang
- SM Devine
- Stephen St. Jeor
- T Tonn
- Y Li
- Y Ye
- Z Selmani
- Publication venue
- Public Library of Science
- Publication date
- 30/05/2012
- Field of study
BACKGROUND: Mesenchymal stem cells (MSC) are promising candidates for cell therapy, as they migrate to areas of injury, differentiate into a broad range of specialized cells, and have immunomodulatory properties. However, MSC are not invisible to the recipient's immune system, and upon in vivo administration, allogeneic MSC are able to trigger immune responses, resulting in rejection of the transplanted cells, precluding their full therapeutic potential. Human cytomegalovirus (HCMV) has developed several strategies to evade cytotoxic T lymphocyte (CTL) and Natural Killer (NK) cell recognition. Our goal is to exploit HCMV immunological evasion strategies to reduce MSC immunogenicity. METHODOLOGY/PRINCIPAL FINDINGS: We genetically engineered human MSC to express HCMV proteins known to downregulate HLA-I expression, and investigated whether modified MSC were protected from CTL and NK attack. Flow cytometric analysis showed that amongst the US proteins tested, US6 and US11 efficiently reduced MSC HLA-I expression, and mixed lymphocyte reaction demonstrated a corresponding decrease in human and sheep mononuclear cell proliferation. NK killing assays showed that the decrease in HLA-I expression did not result in increased NK cytotoxicity, and that at certain NK∶MSC ratios, US11 conferred protection from NK cytotoxic effects. Transplantation of MSC-US6 or MSC-US11 into pre-immune fetal sheep resulted in increased liver engraftment when compared to control MSC, as demonstrated by qPCR and immunofluorescence analyses. CONCLUSIONS AND SIGNIFICANCE: These data demonstrate that engineering MSC to express US6 and US11 can be used as a means of decreasing recognition of MSC by the immune system, allowing higher levels of engraftment in an allogeneic transplantation setting. Since one of the major factors responsible for the failure of allogeneic-donor MSC to engraft is the mismatch of HLA-I molecules between the donor and the recipient, MSC-US6 and MSC-US11 could constitute an off-the-shelf product to overcome donor-recipient HLA-I mismatch
Increased p53 immunopositivity in anaplastic medulloblastoma and supratentorial PNET is not caused by JC virus
- Author
- A Ariza
- A Ray
- AJ Frank
- AM Adesina
- Aneeka Chaudhry
- AS Burns
- B Krynska
- B Krynska
- BL Padgett
- C Russo
- C Sarkar
- C Wetmore
- CC Yuan
- CG Eberhart
- Charles G Eberhart
- CS McManamy
- D Barel
- DE Rollison
- E Fanning
- E Jaros
- F Giangaspero
- F Lopez-Rios
- GA Lammie
- GM Zu Rhein
- H Hayashi
- J Kononen
- JA Biegel
- JA Kraus
- JY Kim
- K Khalili
- K Nagashima
- K Neben
- Keerti V Shah
- L Del Valle
- Leila Khaki
- M Badiali
- M Matsuda
- MT Giordana
- P Kleihues
- Patti E Gravitt
- R Maestro
- R Miralbell
- Richard W Daniel
- RL Saylors
- RR Arthur
- RT Woodburn
- S Marino
- S Postovsky
- S Weggen
- SG Berrak
- SL Pomeroy
- W Wang
- Y Kinoshita
- Y Taoufik
- YS Ho
- Publication venue
- BioMed Central
- Publication date
- 17/02/2005
- Field of study
BACKGROUND: p53 mutations are relatively uncommon in medulloblastoma, but abnormalities in this cell cycle pathway have been associated with anaplasia and worse clinical outcomes. We correlated p53 protein expression with pathological subtype and clinical outcome in 75 embryonal brain tumors. The presence of JC virus, which results in p53 protein accumulation, was also examined. METHODS: p53 protein levels were evaluated semi-quantitatively in 64 medulloblastomas, 3 atypical teratoid rhabdoid tumors (ATRT), and 8 supratentorial primitive neuroectodermal tumors (sPNET) using immunohistochemistry. JC viral sequences were analyzed in DNA extracted from 33 frozen medulloblastoma and PNET samples using quantitative polymerase chain reaction. RESULTS: p53 expression was detected in 18% of non-anaplastic medulloblastomas, 45% of anaplastic medulloblastomas, 67% of ATRT, and 88% of sPNET. The increased p53 immunoreactivity in anaplastic medulloblastoma, ATRT, and sPNET was statistically significant. Log rank analysis of clinical outcome revealed significantly shorter survival in patients with p53 immunopositive embryonal tumors. No JC virus was identified in the embryonal brain tumor samples, while an endogenous human retrovirus (ERV-3) was readily detected. CONCLUSION: Immunoreactivity for p53 protein is more common in anaplastic medulloblastomas, ATRT and sPNET than in non-anaplastic tumors, and is associated with worse clinical outcomes. However, JC virus infection is not responsible for increased levels of p53 protein
Relation between smoking history and gene expression profiles in lung adenocarcinomas
- Author
- A Bhattacharjee
- A Jemal
- A Spira
- AE Bishop
- AI Saeed
- AM Pastva
- Anna Karlsson
- Annette Salomonsson
- BJ Carolan
- CM Bryant
- CM Rudin
- CQ Zhu
- DG Beer
- DN Hayes
- G Jonsson
- Göran Jönsson
- Helen M Pettersson
- J Beane
- J Beane
- J Subramanian
- Johan Staaf
- K Shedden
- K Steiling
- L Ding
- Leif Johansson
- M Lusuardi
- M Ringner
- Maria Planck
- Maria Soller
- Mats Jönsson
- ME Garber
- MT Landi
- Per Jönsson
- R Chari
- R Suzuki
- RH Hubner
- S Sun
- SL Carter
- Sofi Isaksson
- Sven-Börje Ewers
- T Takeuchi
- UD Akavia
- VG Tusher
- X Wang
- Y Lu
- Y Strulovici-Barel
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Measurement and interpretation of same-sign W boson pair production in association with two jets in pp collisions at s = 13 TeV with the ATLAS detector
- Author
- Aad G
- Abbott B
- Abeling K
- Abicht NJ
- Abidi SH
- Aboulhorma A
- Abramowicz H
- Abreu H
- Abulaiti Y
- Abusleme Hoffman AC
- Acharya BS
- Adam Bourdarios C
- Adamczyk L
- Adamek L
- Addepalli SV
- Addison MJ
- Adelman J
- Adiguzel A
- Adye T
- Affolder AA
- Afik Y
- Agaras MN
- Agarwala J
- Aggarwal A
- Agheorghiesei C
- Ahmad A
- Ahmadov F
- Ahmed WS
- Ahuja S
- Ai X
- Aielli G
- Aikot A
- Ait Tamlihat M
- Aitbenchikh B
- Aizenberg I
- Akbiyik M
- Akimov AV
- Akiyama D
- Akolkar NN
- Al Khoury K
- Alberghi GL
- Albert J
- Albicocco P
- Albouy GL
- Alderweireldt S
- Aleksa M
- Aleksandrov IN
- Alexa C
- Alexopoulos T
- Alfonsi F
- Algren M
- Alhroob M
- Ali B
- Ali HMJ
- Ali S
- Alibocus SW
- Aliev M
- Alimonti G
- Alkakhi W
- Allaire C
- Allbrooke BMM
- Allen JF
- Allendes Flores CA
- Allport PP
- Aloisio A
- Alonso F
- Alpigiani C
- Alvarez Estevez M
- Alvarez Fernandez A
- Alves Cardoso M
- Alviggi MG
- Aly M
- Amaral Coutinho Y
- Ambler A
- Amelung C
- Amerl M
- Ames CG
- Amidei D
- Amor Dos Santos SP
- Amos KR
- Ananiev V
- Anastopoulos C
- Andeen T
- Anders JK
- Andrean SY
- Andreazza A
- Angelidakis S
- Angerami A
- Anisenkov AV
- Annovi A
- Antel C
- Anthony MT
- Antipov E
- Antonelli M
- Anulli F
- Aoki M
- Aoki T
- Aparisi Pozo JA
- Aparo MA
- Aperio Bella L
- Appelt C
- Apyan A
- Aranzabal N
- Arcangeletti C
- Arce ATH
- Arena E
- Arguin J-F
- Argyropoulos S
- Arling J-H
- Arnaez O
- Arnold H
- Artoni G
- Asada H
- Asai K
- Asai S
- Asbah NA
- Assamagan K
- Astalos R
- Atashi S
- Atkin RJ
- Atkinson M
- Atmani H
- Atmasiddha PA
- Augsten K
- Auricchio S
- Auriol AD
- Austrup VA
- Avolio G
- Axiotis K
- Azuelos G
- Babal D
- Bachacou H
- Bachas K
- Bachiu A
- Backman F
- Badea A
- Bagnaia P
- Bahmani M
- Bailey AJ
- Bailey VR
- Baines JT
- Baines L
- Bakalis C
- Baker OK
- Bakos E
- Bakshi Gupta D
- Balakrishnan V
- Balasubramanian R
- Baldin EM
- Balek P
- Ballabene E
- Balli F
- Baltes LM
- Balunas WK
- Balz J
- Banas E
- Bandieramonte M
- Bandyopadhyay A
- Bansal S
- Barak L
- Barakat M
- Barberio EL
- Barberis D
- Barbero M
- Barel MZ
- Barends KN
- Barillari T
- Barisits M-S
- Barklow T
- Baron Moreno DA
- Baron P
- Baroncelli A
- Barone G
- Barr AJ
- Barr JD
- Barranco Navarro L
- Barreiro Guimarães da Costa J
- Barreiro F
- Barron U
- Barros Teixeira MG
- Barsov S
- Bartels F
- Bartoldus R
- Barton AE
- Bartos P
- Basan A
- Baselga M
- Bassalat A
- Basso MJ
- Basson CR
- Bates RL
- Batlamous S
- Batley JR
- Batool B
- Battaglia M
- Battulga D
- Bauce M
- Bauer M
- Bauer P
- Bazzano Hurrell LT
- Beacham JB
- Beau T
- Beauchemin PH
- Becherer F
- Bechtle P
- Beck HP
- Becker K
- Becot C
- Beddall AJ
- Bednyakov VA
- Bee CP
- Beemster LJ
- Beermann TA
- Begalli M
- Begel M
- Behera A
- Behr JK
- Beirer JF
- Beisiegel F
- Belfkir M
- Bella G
- Bellagamba L
- Bellerive A
- Bellos P
- Beloborodov K
- Belyaev NL
- Benchekroun D
- Bendebba F
- Benhammou Y
- Benoit M
- Bensinger JR
- Bentvelsen S
- Beresford L
- Beretta M
- Bergeaas Kuutmann E
- Berger N
- Bergmann B
- Beringer J
- Bernardi G
- Bernius C
- Bernlochner FU
- Bernon F
- Berry T
- Berta P
- Berthold A
- Bertram IA
- Bethke S
- Betti A
- Bevan AJ
- Bhamjee M
- Bhatta S
- Bhattacharya DS
- Bhattarai P
- Bhopatkar VS
- Bi R
- Bianchi RM
- Bianco G
- Biebel O
- Bielski R
- Biglietti M
- Billoud TRV
- Bindi M
- Bingul A
- Bini C
- Biondini A
- Birch-sykes CJ
- Bird GA
- Birman M
- Biros M
- Biryukov S
- Bisanz T
- Bisceglie E
- Biswal JP
- Biswas D
- Bitadze A
- Bjørke K
- Bloch I
- Blocker C
- Blue A
- Blumenschein U
- Blumenthal J
- Bobbink GJ
- Bobrovnikov VS
- Boehler M
- Boehm B
- Bogavac D
- Bogdanchikov AG
- Bohm C
- Boisvert V
- Bokan P
- Bold T
- Bomben M
- Bona M
- Boonekamp M
- Booth CD
- Borbély AG
- Bordulev IS
- Borecka-Bielska HM
- Borgna LS
- Borissov G
- Bortoletto D
- Boscherini D
- Bosman M
- Bossio Sola JD
- Bouaouda K
- Bouchhar N
- Boudreau J
- Bouhova-Thacker EV
- Boumediene D
- Bouquet R
- Boveia A
- Boyd J
- Boye D
- Boyko IR
- Bracinik J
- Brahimi N
- Brandt G
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- Braren F
- Brau B
- Brau JE
- Brener R
- Brenner L
- Brenner R
- Bressler S
- Britton D
- Britzger D
- Brock I
- Brooijmans G
- Brooks WK
- Brost E
- Brown LM
- Bruce LE
- Bruckler TL
- Bruckman de Renstrom PA
- Bruni A
- Bruni G
- Bruschi M
- Bruscino N
- Brüers B
- Buanes T
- Buat Q
- Buchin D
- Buckley AG
- Bulekov O
- Bullard BA
- Burdin S
- Burgard CD
- Burger AM
- Burghgrave B
- Burlayenko O
- Burr JTP
- Burton CD
- Burzynski JC
- Busch EL
- Bussey PJ
- Butler JM
- Buttar CM
- Butterworth JM
- Buttinger W
- Buxo Vazquez CJ
- Buzykaev AR
- Büscher V
- Cabrera Urbán S
- Cadamuro L
- Caforio D
- Cai H
- Cai Y
- Cairo VMM
- Cakir O
- Calace N
- Calafiura P
- Calderini G
- Calfayan P
- Callea G
- Caloba LP
- Calvet D
- Calvet S
- Calvet TP
- Calvetti M
- Camacho Toro R
- Camarda S
- Camarero Munoz D
- Camarri P
- Camerlingo MT
- Cameron D
- Camincher C
- Campanelli M
- Camplani A
- Canale V
- Canesse A
- Cantero J
- Cao Y
- Capocasa F
- Capua M
- Carbone A
- Cardarelli R
- Cardenas JCJ
- Cardillo F
- Carli T
- Carlino G
- Carlotto JI
- Carlson BT
- Carlson EM
- Carminati L
- Carnelli A
- Carnesale M
- Caron S
- Carquin E
- Carratta G
- Carrio Argos F
- Carrá S
- Carter JWS
- Carter TM
- Casado MP
- Caspar M
- Castiglia EG
- Castillo Garcia L
- Castillo Gimenez V
- Castillo FL
- Castro NF
- Catinaccio A
- Catmore JR
- Cavaliere V
- Cavalli N
- Cavasinni V
- Cekmecelioglu YC
- Celebi E
- Celli F
- Centonze MS
- Cepaitis V
- Cerny K
- Cerqueira AS
- Cerri A
- Cerrito L
- Cerutti F
- Cervato B
- Cervelli A
- Cesarini G
- Cetin SA
- Chadi Z
- Chakraborty D
- Chan J
- Chan WY
- Chapman JD
- Chapon E
- Chargeishvili B
- Charlton DG
- Charman TP
- Chatterjee M
- Chauhan C
- Chekanov S
- Chekulaev SV
- Chelkov GA
- Chen A
- Chen B
- Chen B
- Chen H
- Chen H
- Chen J
- Chen J
- Chen M
- Chen S
- Chen SJ
- Chen X
- Chen X
- Chen Y
- Cheng CL
- Cheng HC
- Cheong S
- Cheplakov A
- Cheremushkina E
- Cherepanova E
- Cherkaoui El Moursli R
- Cheu E
- Cheung K
- Chevalier L
- Chiarella V
- Chiarelli G
- Chiedde N
- Chiodini G
- Chisholm AS
- Chitan A
- Chitishvili M
- Chizhov MV
- Choi K
- Chomont AR
- Chou Y
- Chow EYS
- Chowdhury T
- Chu KL
- Chu MC
- Chu X
- Chudoba J
- Chwastowski JJ
- Cieri D
- Ciesla KM
- Cindro V
- Ciocio A
- Cirotto F
- Citron ZH
- Citterio M
- Ciubotaru DA
- Ciungu BM
- Clark A
- Clark PJ
- Clavijo Columbie JM
- Clawson SE
- Clement C
- Clercx J
- Coadou Y
- Cobal M
- Coccaro A
- Coelho Barrue RF
- Coelho Lopes De Sa R
- Coelli S
- Cohen H
- Coimbra AEC
- Cole B
- Collot J
- Conde Muiño P
- Connell MP
- Connell SH
- Connelly IA
- Conroy EI
- Conventi F
- Cooke HG
- Cooper-Sarkar AM
- Cordeiro Oudot Choi A
- Cormier F
- Corpe LD
- Corradi M
- Corriveau F
- Cortes-Gonzalez A
- Costa MJ
- Costanza F
- Costanzo D
- Cote BM
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- Soldatov EY
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- Solodkov AA
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- Solovyanov OV
- Solovyev V
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- Sopczak A
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- Tafirout R
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- Talyshev AA
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- Tanaka A
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- Trischuk DA
- Trocmé B
- Troncon C
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- Tsukerman II
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- Vasquez GA
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- Veatch J
- Vecchio V
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- Vermeulen JC
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- Vgenopoulos A
- Viaux Maira N
- Vickey Boeriu OE
- Vickey T
- Viehhauser GHA
- Vigani L
- Villa M
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- Villhauer EM
- Vilucchi E
- Vincter MG
- Virdee GS
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- Visibile A
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- Vladimirov V
- Voevodina E
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- Weingarten J
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- Wiedenmann W
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- Wiglesworth C
- Wilbern DJ
- Wilkens HG
- Williams DM
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- Williams S
- Willocq S
- Wilson BJ
- Windischhofer PJ
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- Winter BT
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- Wobisch M
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- Yabsley B
- Yacoob S
- Yamaguchi Y
- Yamashita E
- Yamauchi H
- Yamazaki T
- Yamazaki Y
- Yan J
- Yan S
- Yan Z
- Yang HJ
- Yang HT
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- Yang Y
- Yang Y
- Yang Z
- Yao W-M
- Yap YC
- Ye H
- Ye H
- Ye J
- Ye S
- Ye X
- Yeh Y
- Yeletskikh I
- Yeo BK
- Yexley MR
- Yin P
- Yorita K
- Younas S
- Young C
- Young CJS
- Yu C
- Yu Y
- Yuan M
- Yuan R
- Yue L
- Zaazoua M
- Zabinski B
- Zaid E
- Zakareishvili T
- Zakharchuk N
- Zambito S
- Zamora Saa JA
- Zang J
- Zanzi D
- Zaplatilek O
- Zeitnitz C
- Zeng H
- Zeng JC
- Zenger DT
- Zenin O
- Zenz S
- Zerradi S
- Zerwas D
- Zhai M
- Zhang B
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- Zhang K
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- Zhang R
- Zhang S
- Zhang T
- Zhang X
- Zhang X
- Zhang Y
- Zhang Y
- Zhang Z
- Zhang Z
- Zhao H
- Zhao P
- Zhao T
- Zhao Y
- Zhao Z
- Zhemchugov A
- Zheng J
- Zheng K
- Zheng X
- Zheng Z
- Zhong D
- Zhou B
- Zhou H
- Zhou N
- Zhou Y
- Zhu CG
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- Zhu Y
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- Zhulanov V
- Zimine NI
- Zinsser J
- Ziolkowski M
- Zoccoli A
- Zoch K
- Zorbas TG
- Zormpa O
- Zou W
- Zwalinski L
- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- Springer Nature
- Publication date
- 01/04/2024
- Field of study
This paper presents the measurement of fducial and diferential cross sections for both the inclusive and electroweak production of a same-sign W-boson pair in association with two jets (W±W±jj) using 139 fb−1 of proton-proton collision data recorded at a centre-of-mass energy of √s = 13 TeV by the ATLAS detector at the Large Hadron Collider. The analysis is performed by selecting two same-charge leptons, electron or muon, and at least two jets with large invariant mass and a large rapidity diference. The measured fducial cross sections for electroweak and inclusive W±W±jj production are 2.92 ± 0.22 (stat.) ± 0.19 (syst.)fb and 3.38±0.22 (stat.)±0.19 (syst.)fb, respectively, in agreement with Standard Model predictions. The measurements are used to constrain anomalous quartic gauge couplings by extracting 95% confdence level intervals on dimension-8 operators. A search for doubly charged Higgs bosons H±± that are produced in vector-boson fusion processes and decay into a same-sign W boson pair is performed. The largest deviation from the Standard Model occurs for an H±± mass near 450 GeV, with a global signifcance of 2.5 standard deviations
Combination of searches for heavy spin-1 resonances using 139 fb−1 of proton-proton collision data at s = 13 TeV with the ATLAS detector
- Author
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- Aakvaag E
- Abbott B
- Abeling K
- Abicht NJ
- Abidi SH
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- Abramowicz H
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- Zhang X
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- Zhang Y
- Zhang Z
- Zhang Z
- Zhao H
- Zhao T
- Zhao Y
- Zhao Z
- Zhao Z
- Zhemchugov A
- Zheng J
- Zheng K
- Zheng X
- Zheng Z
- Zhong D
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- Zhu CG
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- Zhu Y
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- Zhuang X
- Zhukov K
- Zimine NI
- Zinsser J
- Ziolkowski M
- Zoccoli A
- Zoch K
- Zorbas TG
- Zormpa O
- Zou W
- Zwalinski L
- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- Springer Nature
- Publication date
- 19/04/2024
- Field of study
A combination of searches for new heavy spin-1 resonances decaying into different pairings of W, Z, or Higgs bosons, as well as directly into leptons or quarks, is presented. The data sample used corresponds to 139 fb−1 of proton-proton collisions at
= 13 TeV collected during 2015–2018 with the ATLAS detector at the CERN Large Hadron Collider. Analyses selecting quark pairs (qq, bb,
, and tb) or third-generation leptons (τν and ττ) are included in this kind of combination for the first time. A simplified model predicting a spin-1 heavy vector-boson triplet is used. Cross-section limits are set at the 95% confidence level and are compared with predictions for the benchmark model. These limits are also expressed in terms of constraints on couplings of the heavy vector-boson triplet to quarks, leptons, and the Higgs boson. The complementarity of the various analyses increases the sensitivity to new physics, and the resulting constraints are stronger than those from any individual analysis considered. The data exclude a heavy vector-boson triplet with mass below 5.8 TeV in a weakly coupled scenario, below 4.4 TeV in a strongly coupled scenario, and up to 1.5 TeV in the case of production via vector-boson fusion
Allele-Independent Turnover of Human Leukocyte Antigen (HLA) Class Ia Molecules.
- Author
- A De Riva
- A De Riva
- A Neisig
- A Ridley
- AG Grandea 3rd
- AL Ackerman
- Aleksandra M. Gumienny
- AM Andres
- Anna Carla Goldberg
- B Sadasivan
- C Hermann
- C Prevosto
- C Rene
- Ca Peh
- CJ Barnstable
- Claudia Prevosto
- CS Falk
- DC Chapman
- DM Evans
- DR Johnson
- E Reeves
- ET Spiliotis
- EY Jones
- F Cano
- F Momburg
- F Sallusto
- GE Hammer
- H Rabenstein
- HG Rammensee
- HG Rivas
- HP Koeffler
- HT Orr
- I Teobald
- J Neefjes
- J Robinson
- J. S. Hill Gaston
- JE McLaren
- JJ Neefjes
- JJ Neefjes
- JS Blum
- K Kärre
- K Murphy
- KW Jorgensen
- L Li
- LG Spurgin
- LL Lanier
- LM Dobbe
- LM Duncan
- M Cella
- M Gromme
- M Rowe
- M. Farooq Usmani
- MA Garstka
- Michael J. Deery
- MK Hellerstein
- ML DeLay
- ML van de Weijer
- ML Wei
- MR Schaefer
- MR Wilkins
- MT Barel
- N Rachdaoui
- O Chazara
- P Bowness
- PJ Bjorkman
- PJ van den Elsen
- R Apps
- R Obst
- RD Salter
- RE Hammer
- Reyna S. Goodman
- Robert Busch
- S Gras
- S Kulkarni
- Sarah McDonald
- SG Santos
- T Hou
- Tim Key
- TY Kim
- V Thammavongsa
- V Thammavongsa
- WE Holmes
- Y Shimizu
- Publication venue
- PLoS One
- Publication date
- 01/01/2016
- Field of study
Major histocompatibility complex class I (MHCI) glycoproteins present cytosolic peptides to CD8+ T cells and regulate NK cell activity. Their heavy chains (HC) are expressed from up to three MHC gene loci (human leukocyte antigen [HLA]-A, -B, and -C in humans), whose extensive polymorphism maps predominantly to the antigen-binding groove, diversifying the bound peptide repertoire. Codominant expression of MHCI alleles is thus functionally critical, but how it is regulated is not fully understood. Here, we have examined the effect of polymorphism on the turnover rates of MHCI molecules in cell lines with functional MHCI peptide loading pathways and in monocyte-derived dendritic cells (MoDCs). Proteins were labeled biosynthetically with heavy water (2H2O), folded MHCI molecules immunoprecipitated, and tryptic digests analysed by mass spectrometry. MHCI-derived peptides were assigned to specific alleles and isotypes, and turnover rates quantified by 2H incorporation, after correcting for cell growth. MHCI turnover half-lives ranged from undetectable to a few hours, depending on cell type, activation state, donor, and MHCI isotype. However, in all settings, the turnover half-lives of alleles of the same isotype were similar. Thus, MHCI protein turnover rates appear to be allele-independent in normal human cells. We propose that this is an important feature enabling the normal function and codominant expression of MHCI alleles
Combined measurement of the Higgs boson mass from the H → γγ and H → ZZ∗ → 4ℓ decay channels with the ATLAS detector using √s = 7, 8, and 13 TeV pp collision data
- Author
- Aad G
- Abbott B
- Abeling K
- Abicht NJ
- Abidi SH
- Aboulhorma A
- Abramowicz H
- Abreu H
- Abulaiti Y
- Acharya BS
- Adam Bourdarios C
- Adamczyk L
- Addepalli SV
- Addison MJ
- Adelman J
- Adiguzel A
- Adye T
- Affolder AA
- Afik Y
- Agaras MN
- Agarwala J
- Aggarwal A
- Agheorghiesei C
- Ahmad A
- Ahmadov F
- Ahmed WS
- Ahuja S
- Ai X
- Aielli G
- Aikot A
- Ait Tamlihat M
- Aitbenchikh B
- Aizenberg I
- Akbiyik M
- Akimov AV
- Akiyama D
- Akolkar NN
- Al Khoury K
- Alberghi GL
- Albert J
- Albicocco P
- Albouy GL
- Alderweireldt S
- Aleksa M
- Aleksandrov IN
- Alexa C
- Alexopoulos T
- Alfonsi F
- Algren M
- Alhroob M
- Ali B
- Ali HMJ
- Ali S
- Alibocus SW
- Aliev M
- Alimonti G
- Alkakhi W
- Allaire C
- Allbrooke BMM
- Allen JF
- Allendes Flores CA
- Allport PP
- Aloisio A
- Alonso F
- Alpigiani C
- Alvarez Estevez M
- Alvarez Fernandez A
- Alves Cardoso M
- Alviggi MG
- Aly M
- Amaral Coutinho Y
- Ambler A
- Amelung C
- Amerl M
- Ames CG
- Amidei D
- Amor Dos Santos SP
- Amos KR
- Ananiev V
- Anastopoulos C
- Andeen T
- Anders JK
- Andrean SY
- Andreazza A
- Angelidakis S
- Angerami A
- Anisenkov AV
- Annovi A
- Antel C
- Anthony MT
- Antipov E
- Antonelli M
- Anulli F
- Aoki M
- Aoki T
- Aparisi Pozo JA
- Aparo MA
- Aperio Bella L
- Appelt C
- Apyan A
- Aranzabal N
- Arbiol Val SJ
- Arcangeletti C
- Arce ATH
- Arena E
- Arguin J-F
- Argyropoulos S
- Arling J-H
- Arnaez O
- Arnold H
- Artoni G
- Asada H
- Asai K
- Asai S
- Asbah NA
- Assahsah J
- Assamagan K
- Astalos R
- Atashi S
- Atkin RJ
- Atkinson M
- ATLAS Collaboration
- Atmani H
- Atmasiddha PA
- Augsten K
- Auricchio S
- Auriol AD
- Austrup VA
- Avolio G
- Axiotis K
- Azuelos G
- Babal D
- Bachacou H
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- Bachiu A
- Backman F
- Badea A
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- Bailey AJ
- Bailey VR
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- Baker OK
- Bakos E
- Bakshi Gupta D
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- Balasubramanian R
- Baldin EM
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- Bandyopadhyay A
- Bansal S
- Barak L
- Barakat M
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- Barends KN
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- Barklow T
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- Baroncelli A
- Barone G
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- Barr JD
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- Barreiro Guimarães da Costa J
- Barreiro F
- Barron U
- Barros Teixeira MG
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- Bartoldus R
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- Basson CR
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- Batley JR
- Batool B
- Battaglia M
- Battulga D
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- Bauer M
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- Bazzano Hurrell LT
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- Beaucamp JY
- Beauchemin PH
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- Beddall AJ
- Bednyakov VA
- Bee CP
- Beemster LJ
- Beermann TA
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- Birch-Sykes CJ
- Bird GA
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- Zhang T
- Zhang X
- Zhang X
- Zhang Y
- Zhang Y
- Zhang Y
- Zhang Z
- Zhang Z
- Zhao H
- Zhao P
- Zhao T
- Zhao Y
- Zhao Z
- Zhemchugov A
- Zheng J
- Zheng K
- Zheng X
- Zheng Z
- Zhong D
- Zhou B
- Zhou H
- Zhou N
- Zhou Y
- Zhu CG
- Zhu J
- Zhu Y
- Zhu Y
- Zhuang X
- Zhukov K
- Zhulanov V
- Zimine NI
- Zinsser J
- Ziolkowski M
- Zoccoli A
- Zoch K
- Zorbas TG
- Zormpa O
- Zou W
- Zwalinski L
- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- American Physical Society
- Publication date
- 01/01/2023
- Field of study
A measurement of the mass of the Higgs boson combining the
H
→
Z
Z
∗
→
4
ℓ
and
H
→
γ
γ
decay channels is presented. The result is based on
140
fb
−
1
of proton-proton collision data collected by the ATLAS detector during LHC run 2 at a center-of-mass energy of 13 TeV combined with the run 1 ATLAS mass measurement, performed at center-of-mass energies of 7 and 8 TeV, yielding a Higgs boson mass of
125.11
±
0.09
(
stat
)
±
0.06
(
syst
)
=
125.11
±
0.11
GeV
. This corresponds to a 0.09% precision achieved on this fundamental parameter of the Standard Model of particle physics
- …