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Hamilton JD, Suarez-Farinas M, Dhingra N, Cardinale I, Li X, Kostic A, Ming JE, Radin AR, Krueger JG, Graham N, Yancopoulos GD, Pirozzi G, Guttman-Yassky E
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Dupilumab improves the molecular signature in skin of patients with moderate-to-severe atopic dermatitis
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY 2014 DEC; 134(6):1293-1300
Background: Severe atopic dermatitis (AD) has a high unmet need for effective and safe therapeutics. In early-phase trials, dupilumab, a fully human mAb targeting IL-4 receptor alpha, markedly improved disease activity, but the effect of IL-4/IL-13 blockade on AD at the molecular level has not been characterized. Objectives: We sought to evaluate dupilumab modulation of the AD molecular signature. Methods: We performed transcriptomic analyses of pretreatment and posttreatment skin biopsy specimens from patients with moderate-to-severe AD treated weekly with 150 or 300 mg of dupilumab or placebo. Results: Exacerbation of the AD transcriptome was observed in placebo-treated patients. Dupilumab improved the AD signature in a dose-dependent manner. Expression of genes upregulated in AD lesions decreased in patients treated with dupilumab by 26% (95% CI, 21% to 32%) and 65% (95% CI, 60% to 71%) for treatment with 150 and 300 mg, respectively. Genes downregulated in AD lesions increased by 21% (95% CI, 16% to 27%) and 32% (95% CI, 26% to 37%) with dupilumab (150 and 300 mg, respectively). The molecular changes paralleled improvements in clinical scores. A dupilumab treatment signature of 821 probes (>2-fold change, P < .05) significantly modulated in the 300-mg dupilumab group at week 4 compared with baseline was identified in this sample set. Significant (P < .05) decreases in mRNA expression of genes related to hyperplasia (K16 and MKI67), T cells, and dendritic cells (CD1b and CD1c) and potent inhibition of T(H)2-associated chemokines (CCL17, CCL18, CCL22, and CCL26) were noted without significant modulation of T(H)1-associated genes (IFNG). Conclusions: This is the first report showing rapid improvement of the AD molecular signature with targeted anti-IL-4 receptor a therapy. These data suggest that IL-4 and IL-13 drive a complex, T(H)2-centered inflammatory axis in patients with AD.
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Search for pair production of third-generation scalar leptoquarks and top squarks in proton-proton collisions at v root s=8 TeV
PHYSICS LETTERS B 2014 DEC 12; 739(?):229-249
A search for pair production of third-generation scalar leptoquarks and supersymmetric top quark partners, top squarks, in final states involving tau leptons and bottom quarks is presented. The search uses events from a data sample of proton-proton collisions corresponding to an integrated luminosity of 19.7 fb(-1), collected with the CMS detector at the LHC with root s = 8 TeV. The number of observed events is found to be in agreement with the expected standard model background. Third-generation scalar leptoquarks with masses below 740 GeV are excluded at 95% confidence level, assuming a 100% branching fraction for the leptoquark decay to a tau lepton and a bottom quark. In addition, this mass limit applies directly to top squarks decaying via an R-parity violating coupling. lambda(') (333). The search also considers a similar signature from top squarks undergoing a chargino-mediated decay involving the Rparity violating coupling. lambda(')(3jk). Each top squark decays to a tau lepton, a bottom quark, and two light quarks. Top squarks in this model with masses below 580 GeV are excluded at 95% confidence level. The constraint on the leptoquark mass is the most stringent to date, and this is the first search for top squarks decaying via. lambda(')(3jk). (C) 2014 The Authors. Published by Elsevier B. V.
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Faccioli P, Parracho PGF, Gallinaro M, Nguyen F, Antunes JR, Seixas J, Varela J, Vischia P, Afanasiev S, Gavrilenko M, Golutvin I, Kamenev A, Karjavin V, Konoplyanikov V, Lanev A, Malakhov A, Matveev V, Moisenz P, Palichik V, Perelygin V, Savina M, Shmatov S, Shulha S, Skatchkov N, Smirnov V, Zarubin A, Golovtsov V, Ivanov Y, Kim V, Levchenko P, Murzin V, Oreshkin V, Smirnov I, Sulimov V, Uvarov L, Vavilov S, Vorobyev A, Vorobyev A, Andreev Y, Dermenev A, Gninenko S, Golubev N, Kirsanov M, Krasnikov N, Pashenkov A, Tlisov D, Toropin A, Epshteyn V, Gavrilov V, Lychkovskaya N, Popov V, Safronov G, Semenov S, Spiridonov A, Stolin V, Vlasov E, Zhokin A, Andreev V, Azarkin M, Dremin I, Kirakosyan M, Leonidov A, Mesyats G, Rusakov SV, Vinogradov A, Belyaev A, Boos E, Bunichev V, Dubinin M, Dudko L, Ershov A, Klyukhin V, Kodolova O, Lokhtin I, Obraztsov S, Petrushanko S, Savrin V, Snigirev A, Azhgirey I, Bayshev I, Bitioukov S, Kachanov V, Kalinin A, Konstantinov D, Krychkine V, Petrov V, Ryutin R, Sobol A, Tourtchanovitch L, Troshin S, Tyurin N, Uzunian A, Volkov A, Adzic P, Ekmedzic M, Milosevic J, Rekovic V, Maestre JA, Battilana C, Calvo E, Cerrada M, Llatas MC, Colino N, De La Cruz B, Peris AD, Vazquez DD, Del Valle AE, Bedoya CF, Ramos JPF, Flix J, Fouz MC, Garcia-Abia P, Lopez OG, Lopez SG, Hernandez JM, Josa MI, Merino G, De Martino EN, Yzquierdo APC, Pelayo JP, Olmeda AQ, Redondo I, Romero L, Soares MS, Albajar C, de Troconiz JF, Missiroli M, Moran D, Brun H, Cuevas J, Menendez JF, Folgueras S, Caballero IG, Iglesias LL, Cifuentes JAB, Cabrillo IJ, Calderon A, Campderros JD, Fernandez M, Gomez G, Graziano A, Virto AL, Marco J, Marco R, Rivero CM, Matorras F, Sanchez FJM, Gomez JP, Rodrigo T, Rodriguez-Marrero AY, Ruiz-Jimeno A, Scodellaro L, Vila I, Cortabitarte RV, Abbaneo D, Auffray E, Auzinger G, Bachtis M, Baillon P, Ball AH, Barney D, Benaglia A, Bendavid J, Benhabib L, Benitez JF, Bernet C, Bianchi G, Bloch P, Bocci A, Bonato A, Bondu O, Botta C, Breuker H, Camporesi T, Cerminara G, Colafranceschi S, D'Alfonso M, d'Enterria D, Dabrowski A, David A, De Guio F, De Roeck A, De Visscher S, Dobson M, Dordevic M, Dupont-Sagorin N, Elliott-Peisert A, Eugster J, Franzoni G, Funk W, Gigi D, Gill K, Giordano D, Girone M, Glege F, Guida R, Gundacker S, Guthoff M, Hammer J, Hansen M, Harris P, Hegeman J, Innocente V, Janot P, Kousouris K, Krajczar K, Lecoq P, Lourenco C, Magini N, Malgeri L, Mannelli M, Marrouche J, Masetti L, Meijers F, Mersi S, Meschi E, Moortgat F, Morovic S, Mulders M, Musella P, Orsini L, Pape L, Perez E, Perrozzi L, Petrilli A, Petrucciani G, Pfeiffer A, Pierini M, Pimia M, Piparo D, Plagge M, Racz A, Rolandi G, Rovere M, Sakulin H, Schafer C, Schwick C, Sharma A, Siegrist P, Silva P, Simon M, Sphicas P, Spiga D, Steggemann J, Stieger B, Stoye M, Treille D, Tsirou A, Veres GI, Vlimant JR, Wardle N, Wohri HK, Wollny H, Zeuner WD, Bertl W, Deiters K, Erdmann W, Horisberger R, Ingram Q, Kaestli HC, Kotlinski D, Langenegger U, 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Polatoz A, Sogut K, Cerci DS, Tali B, Topakli H, Vergili M, Akin IV, Bilin B, Bilmis S, Gamsizkan H, Karapinar G, Ocalan K, Sekmen S, Surat UE, Yalvac M, Zeyrek M, Gulmez E, Isildak B, Kaya M, Kaya O, Bahtiyar H, Barlas E, Cankocak K, Vardarli FI, Yucel M, Levchuk L, Sorokin P, Brooke JJ, Clement E, Cussans D, Flacher H, Frazier R, Goldstein J, Grimes M, Heath GP, Heath HF, Jacob J, Kreczko L, Lucas C, Meng Z, Newbold DM, Paramesvaran S, Poll A, Senkin S, Smith VJ, Williams T, Bell KW, Belyaev A, Brew C, Brown RM, Cockerill DJA, Coughlan JA, Harder K, Harper S, Olaiya E, Petyt D, Shepherd-Themistocleous CH, Thea A, Tomalin IR, Womersley WJ, Worm SD, Baber M, Bainbridge R, Buchmuller O, Burton D, Colling D, Cripps N, Cutajar M, Dauncey P, Davies G, Della Negra M, Dunne P, Ferguson W, Fulcher J, Futyan D, Gilbert A, Hall G, Iles G, Jarvis M, Karapostoli G, Kenzie M, Lane R, Lucas R, Lyons L, Magnan AM, Malik S, Mathias B, Nash J, Nikitenko A, Pela J, Pesaresi M, Petridis K, Raymond DM, Rogerson S, Rose A, Seez C, Sharp P, Tapper A, Acosta MV, Virdee T, Cole JE, Hobson PR, Khan A, Kyberd P, Leggat D, Leslie D, Martin W, Reid ID, Symonds P, Teodorescu L, Turner M, Dittmann J, Hatakeyama K, Kasmi A, Liu H, Scarborough T, Charaf O, Cooper SI, Henderson C, Rumerio P, Avetisyan A, Bose T, Fantasia C, Lawson P, Richardson C, Rohlf J, Sperka D, John JS, Sulak L, Alimena J, Berry E, Bhattacharya S, Christopher G, Cutts D, Demiragli Z, Ferapontov A, Garabedian A, Heintz U, Kukartsev G, Laird E, Landsberg G, Luk M, Narain M, Segala M, Sinthuprasith T, Speer T, Swanson J, Breedon R, Breto G, Sanchez MCD, Chauhan S, Chertok M, Conway J, Conway R, Cox PT, Erbacher R, Gardner M, Ko W, Lander R, Miceli T, Mulhearn M, Pellett D, Pilot J, Ricci-Tam F, Searle M, Shalhout S, Smith J, Squires M, Stolp D, Tripathi M, Wilbur S, Yohay R, Cousins R, Everaerts P, Farrell C, Hauser J, Ignatenko M, Rakness G, Takasugi E, Valuev V, Weber M, Babb J, Burt K, Clare R, Ellison J, Gary JW, Hanson G, Heilman J, Rikova MI, Jandir P, Kennedy E, Lacroix F, Liu H, Long OR, Luthra A, Malberti M, Nguyen H, Negrete MO, Shrinivas A, Sumowidagdo S, Wimpenny S, Andrews W, Branson JG, Cerati GB, Cittolin S, D'Agnolo RT, Evans D, Holzner A, Kelley R, Klein D, Lebourgeois M, Letts J, Macneill I, Olivito D, Padhi S, Palmer C, Pieri M, Sani M, Sharma V, Simon S, Sudano E, Tadel M, Tu Y, Vartak A, Welke C, Wurthwein F, Yagil A, Yoo J, Barge D, Bradmiller-Feld J, Campagnari C, Danielson T, Dishaw A, Flowers K, Sevilla MF, Geffert P, George C, Golf F, Gouskos L, Incandela J, Justus C, Mccoll N, Richman J, Stuart D, To W, West C, Apresyan A, Bornheim A, Bunn J, Chen Y, Di Marco E, Duarte J, Mott A, Newman HB, Pena C, Rogan C, Spiropulu M, Timciuc V, Wilkinson R, Xie S, Zhu RY, Azzolini V, Calamba A, Carlson B, Ferguson T, Iiyama Y, Paulini M, Russ J, Vogel H, Vorobiev I, Cumalat JP, Ford WT, Gaz A, Lopez EL, Nauenberg U, Smith JG, Stenson K, Ulmer KA, Wagner SR, Alexander J, Chatterjee A, Chu J, Dittmer S, Eggert N, Mirman N, Kaufman GN, Patterson JR, Ryd A, Salvati E, Skinnari L, Sun W, Teo WD, Thom J, Thompson J, Tucker J, Weng Y, Winstrom L, Wittich P, Winn D, Abdullin S, Albrow M, Anderson J, Apollinari G, Bauerdick LAT, Beretvas A, Berryhill J, Bhat PC, Burkett K, Butler JN, Cheung HWK, Chlebana F, Cihangir S, Elvira VD, Fisk I, Freeman J, Gao Y, Gottschalk E, Gray L, Green D, Grunendahl S, Gutsche O, Hanlon J, Hare D, Harris RM, Hirschauer J, Hooberman B, Jindariani S, Johnson M, Joshi U, Kaadze K, Klima B, Kreis B, Kwan S, Linacre J, Lincoln D, Lipton R, Liu T, Lykken J, Maeshima K, Marraffino JM, Outschoorn VIM, Maruyama S, Mason D, McBride P, Mishra K, Mrenna S, Musienko Y, Nahn S, Newman-Holmes C, O'Dell V, Prokofyev O, Sexton-Kennedy E, Sharma S, Soha A, Spalding WJ, Spiegel L, Taylor L, Tkaczyk S, Tran NV, Uplegger L, Vaandering EW, Vidal R, Whitbeck A, Whitmore J, Yang F, Acosta D, Avery P, Bourilkov D, Carver M, Cheng T, Curry D, Das S, De Gruttola M, Di Giovanni GP, Field RD, Fisher M, Furic IK, Hugon J, Konigsberg J, Korytov A, Kypreos T, Low JF, Matchev K, Milenovic P, Mitselmakher G, Muniz L, Rinkevicius A, Shchutska L, Snowball M, Yelton J, Zakaria M, Hewamanage S, Linn S, Markowitz P, Martinez G, Rodriguez JL, Adams T, Askew A, Bochenek J, Diamond B, Haas J, Hagopian S, Hagopian V, Johnson KF, Prosper H, Veeraraghavan V, Weinberg M, Baarmand MM, Hohlmann M, Kalakhety H, Yumiceva F, Adams MR, Apanasevich L, Bazterra VE, Berry D, Betts RR, Bucinskaite I, Cavanaugh R, Evdokimov O, Gauthier L, Gerber CE, Hofman DJ, Khalatyan S, Kurt P, Moon DH, O'Brien C, Silkworth C, Turner P, Varelas N, Albayrak EA, Bilki B, Clarida W, Dilsiz K, Duru F, Haytmyradov M, Merlo JP, Mermerkaya H, Mestvirishvili A, Moeller A, Nachtman J, Ogul H, Onel Y, Ozok F, Penzo A, Rahmat R, Sen S, Tan P, Tiras E, Wetzel J, Yetkin T, Yi K, Barnett BA, Blumenfeld B, Bolognesi S, Fehling D, Gritsan AV, Maksimovic P, Martin C, Swartz M, Baringer P, Bean A, Benelli G, Bruner C, Gray J, Kenny RP, Malek M, Murray M, Noonan D, Sanders S, Sekaric J, Stringer R, Wang Q, Wood JS, Barfuss AF, Chakaberia I, Ivanov A, Khalil S, Makouski M, Maravin Y, Saini LK, Shrestha S, Skhirtladze N, Svintradze I, Gronberg J, Lange D, Rebassoo F, Wright D, Baden A, Belloni A, Calvert B, Eno SC, Gomez JA, Hadley NJ, Kellogg RG, Kolberg T, Lu Y, Marionneau M, Mignerey AC, Pedro K, Skuja A, Tonjes MB, Tonwar SC, Apyan A, Barbieri R, Bauer G, Busza W, Cali IA, Chan M, Di Matteo L, Dutta V, Ceballos GG, Goncharov M, Gulhan D, Klute M, Lai YS, Lee YJ, Levin A, Luckey PD, Ma T, Paus C, Ralph D, Roland C, Roland G, Stephans GSF, Stockli F, Sumorok K, Velicanu D, Veverka J, Wyslouch B, Yang M, Zanetti M, Zhukova V, Dahmes B, Gude A, Kao SC, Klapoetke K, Kubota Y, Mans J, Pastika N, Rusack R, Singovsky A, Tambe N, Turkewitz J, Acosta JG, Oliveros S, Avdeeva E, Bloom K, Bose S, Claes DR, Dominguez A, Suarez RG, Keller J, Knowlton D, Kravchenko I, Lazo-Flores J, Malik S, Meier F, Snow GR, Dolen J, Godshalk A, Iashvili I, Kharchilava A, Kumar A, Rappoccio S, Alverson G, Barberis E, Baumgartel D, Chasco M, Haley J, Massironi A, Morse DM, Nash D, Orimoto T, Trocino D, Wang RJ, Wood D, Zhang J, Hahn KA, Kubik A, Mucia N, Odell N, Pollack B, Pozdnyakov A, Schmitt M, Stoynev S, Sung K, Velasco M, Won S, Brinkerhoff A, Chan KM, Drozdetskiy A, Hildreth M, Jessop C, Karmgard DJ, Kellams N, Lannon K, Luo W, Lynch S, Marinelli N, Pearson T, Planer M, Ruchti R, Valls N, Wayne M, Wolf M, Woodard A, Antonelli L, Brinson J, Bylsma B, Durkin LS, Flowers S, Hill C, Hughes R, Kotov K, Ling TY, Puigh D, Rodenburg M, Smith G, Winer BL, Wolfe H, Wulsin HW, Driga O, Elmer P, Hebda P, Hunt A, Koay SA, Lujan P, Marlow D, Medvedeva T, Mooney M, Olsen J, Piroue P, Quan X, Saka H, Stickland D, Tully C, Werner JS, Zenz SC, Zuranski A, Brownson E, Mendez H, Vargas JER, Alagoz E, Barnes VE, Benedetti D, Bolla G, Bortoletto D, De Mattia M, Hu Z, Jha MK, Jones M, Jung K, Kress M, Leonardo N, Pegna DL, Maroussov V, Merkel P, Miller DH, Neumeister N, Radburn-Smith BC, Shi X, Shipsey I, Silvers D, Svyatkovskiy A, Wang F, Xie W, Xu L, Yoo HD, Zablocki J, Zheng Y, Parashar N, Stupak J, Adair A, Akgun B, Ecklund KM, Geurts FJM, Li W, Michlin B, Padley BP, Redjimi R, Roberts J, Zabel J, Betchart B, Bodek A, Covarelli R, de Barbaro P, Demina R, Eshaq Y, Ferbel T, Garcia-Bellido A, Goldenzweig P, Han J, Harel A, Khukhunaishvili A, Petrillo G, Vishnevskiy D, Ciesielski R, Demortier L, Goulianos K, Lungu G, Mesropian C, Arora S, Barker A, Chou JP, Contreras-Campana C, Contreras-Campana E, Craig N, Duggan D, Evans J, Ferencek D, Gershtein Y, Gray R, Halkiadakis E, Hidas D, Lath A, Panwalkar S, Park M, Patel R, Salur S, Schnetzer S, Somalwar S, Stone R, Thomas S, Thomassen P, Walker M, Rose K, Spanier S, York A, Bouhali O, Eusebi R, Flanagan W, Gilmore J, Kamon T, Khotilovich V, Krutelyov V, Montalvo R, Osipenkov I, Pakhotin Y, Perloff A, Roe J, Rose A, Safonov A, Sakuma T, Suarez I, Tatarinov A, Akchurin N, Cowden C, Damgov J, Dragoiu C, Dudero PR, Faulkner J, Kovitanggoon K, Kunori S, Lee SW, Libeiro T, Volobouev I, Appelt E, Delannoy AG, Greene S, Gurrola A, Johns W, Maguire C, Mao Y, Melo A, Sharma M, Sheldon P, Snook B, Tuo S, Velkovska J, Arenton MW, Boutle S, Cox B, Francis B, Goodell J, Hirosky R, Ledovskoy A, Li H, Lin C, Neu C, Wood J, Clarke C, Harr R, Karchin PE, Don CKK, Lamichhane P, Sturdy J, Belknap DA, Carlsmith D, Cepeda M, Dasu S, Dodd L, Duric S, Friis E, Hall-Wilton R, Herndon M, Herve A, Klabbers P, Lanaro A, Lazaridis C, Levine A, Loveless R, Mohapatra A, Ojalvo I, Perry T, Pierro GA, Polese G, Ross I, Sarangi T, Savin A, Smith WH, Vuosalo C, Woods N
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Searches for heavy Higgs bosons in two-Higgs-doublet models and for t -> ch decay using multilepton and diphoton final states in pp collisions at 8 TeV
PHYSICAL REVIEW D 2014 DEC 23; 90(11):? Article 112013
Searches are presented for heavy scalar (H) and pseudoscalar (A) Higgs bosons posited in the two doublet model (2HDM) extensions of the standard model (SM). These searches are based on a data sample of pp collisions collected with the CMS experiment at the LHC at a center-of-mass energy of root s = 8 TeV and corresponding to an integrated luminosity of 19.5 fb(-1). The decays H -> hh and A -> Zh, where h denotes an SM-like Higgs boson, lead to events with three or more isolated charged leptons or with a photon pair accompanied by one or more isolated leptons. The search results are presented in terms of the H and A production cross sections times branching fractions and are further interpreted in terms of 2HDM parameters. We place 95% C.L. cross section upper limits of approximately 7 pb on sigma B for H -> hh and 2 pb for A -> Zh. Also presented are the results of a search for the rare decay of the top quark that results in a charm quark and an SM Higgs boson, t -> ch, the existence of which would indicate a nonzero flavor-changing Yukawa coupling of the top quark to the Higgs boson. We place a 95% C.L. upper limit of 0.56% on B(t -> ch).
Meng FL, Du Z, Federation A, Hu JZ, Wang Q, Kieffer-Kwon KR, Meyers RM, Amor C, Wasserman CR, Neuberg D, Casellas R, Nussenzweig MC, Bradner JE, Liu XS, Alt FW
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Convergent Transcription at Intragenic Super-Enhancers Targets AID-Initiated Genomic Instability
CELL 2014 DEC 18; 159(7):1538-1548
Activation-induced cytidine deaminase (AID) initiates both somatic hypermutation (SHM) for antibody affinity maturation and DNA breakage for antibody class switch recombination (CSR) via transcription-dependent cytidine deamination of single-stranded DNA targets. Though largely specific for immunoglobulin genes, AID also acts on a limited set of off-targets, generating oncogenic translocations and mutations that contribute to B cell lymphoma. How AID is recruited to off-targets has been a long-standing mystery. Based on deep GRO-seq studies of mouse and human B lineage cells activated for CSR or SHM, we report that most robust AID off-target translocations occur within highly focal regions of target genes in which sense and antisense transcription converge. Moreover, we found that such AID-targeting "convergent'' transcription arises from antisense transcription that emanates from super-enhancers within sense transcribed gene bodies. Our findings provide an explanation for AID off-targeting to a small subset of mostly lineage-specific genes in activated B cells.
Roy AL, Roeder RG
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Cnromatin and transcriptional tango on the immune dance floor
FRONTIERS IN IMMUNOLOGY 2014 DEC 15; 5(?):?
Lu CC, Wu TS, Hsu YJ, Chang CJ, Lin CS, Chia JH, Wu TL, Huang TT, Martel J, Ojcius DM, Young JD, Lai HC
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NK cells kill mycobacteria directly by releasing perforin and granulysin
JOURNAL OF LEUKOCYTE BIOLOGY 2014 DEC; 96(6):1119-1129
NK cells directly kill mycobacteria through a contactdependent mechanism leading to the release of perforin and granulysin. Although the mechanisms underlying the cytotoxic effect of NK cells on tumor cells and intracellular bacteria have been studied extensively, it remains unclear how these cells kill extracellular bacterial pathogens. In this study, we examine how human NK cells kill Mycobacterium kansasii and M.tb. The underlying mechanism is contact dependent and requires two cytolytic proteins: perforin and granulysin. Mycobacteria induce enhanced expression of the cytolytic proteins via activation of the NKG2D/NCR cell-surface receptors and intracellular signaling pathways involving ERK, JNK, and p38 MAPKs. These results suggest that NK cells use similar cellular mechanisms to kill both bacterial pathogens and target host cells. This report reveals a novel role for NK cells, perforin, and granulysin in killing mycobacteria and highlights a potential alternative defense mechanism that the immune system can use against mycobacterial infection.
Gore AC, Martien KM, Gagnidze K, Pfaff D
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Implications of Prenatal Steroid Perturbations for Neurodevelopment, Behavior, and Autism
ENDOCRINE REVIEWS 2014 DEC; 35(6):961-991
The prenatal brain develops under the influence of an ever-changing hormonal milieu that includes endogenous fetal gonadal and adrenal hormones, placental and maternal hormones, and exogenous substances with hormonal activity that can cross the placental barrier. This review discusses the influences of endogenous fetal and maternal hormones on normal brain development and potential consequences of pathophysiological hormonal perturbations to the developing brain, with particular reference to autism. We also consider the effects of hormonal pharmaceuticals used for assisted reproduction, the maintenance of pregnancy, the prevention of congenital adrenal hypertrophy, and hormonal contraceptives continued into an unanticipated pregnancy, amongothers. These treatments, although in some instances life-saving, may have unintended consequences on the developing fetuses. Additional concern is raised by fetal exposures to endocrine-disrupting chemicals encountered universally by pregnant women from food/water containers, contaminated food, household chemicals, and other sources. What are the potential outcomes of prenatal steroid perturbations on neurodevelopmental and behavioral disorders, including autismspectrum disorders? Our purposes here are 1) to summarize some consequences of steroid exposures during pregnancy for the development of brain and behavior in the offspring; 2) to summarize what is known about the relationships between exposures and behavior, including autism spectrum disorders; 3) to discuss the molecular underpinnings of such effects, especially molecular epigenetic mechanisms of prenatal steroid manipulations, a field that may explain effects of direct exposures, and even transgenerational effects; and 4) for all of these, to add cautionary notes about their interpretation in the name of scientific rigor.
Sagi Y, Heiman M, Peterson JD, Musatov S, Kaplitt MG, Surmeier DJ, Heintz N, Greengard P
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Nitric oxide regulates synaptic transmission between spiny projection neurons
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2014 DEC 9; 111(49):17636-17641
Recurrent axon collaterals are a major means of communication between spiny projection neurons (SPNs) in the striatum and profoundly affect the function of the basal ganglia. However, little is known about the molecular and cellular mechanisms that underlie this communication. We show that intrastriatal nitric oxide (NO) signaling elevates the expression of the vesicular GABA transporter (VGAT) within recurrent collaterals of SPNs. Down-regulation of striatal NO signaling resulted in an attenuation of GABAergic signaling in SPN local collaterals, down-regulation of VGAT expression in local processes of SPNs, and impaired motor behavior. PKG1 and cAMP response element-binding protein are involved in the signal transduction that transcriptionally regulates VGAT by NO. These data suggest that transcriptional control of the vesicular GABA transporter by NO regulates GABA transmission and action selection.
McGuire AT, Dreyer AM, Carbonetti S, Lippy A, Glenn J, Scheid JF, Mouquet H, Stamatatos L
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Antigen modification regulates competition of broad and narrow neutralizing HIV antibodies
SCIENCE 2014 DEC 12; 346(6215):1380-1383
Some HIV-infected individuals develop broadly neutralizing antibodies (bNAbs), whereas most develop antibodies that neutralize only a narrow range of viruses (nNAbs). bNAbs, but not nNAbs, protect animals from experimental infection and are likely a key component of an effective vaccine. nNAbs and bNAbs target the same regions of the viral envelope glycoprotein (Env), but for reasons that remain unclear only nNAbs are elicited by Env immunization. We show that in contrast to germline-reverted (gl) bNAbs, glnNAbs recognized diverse recombinant Envs. Moreover, owing to binding affinity differences, nNAb B cell progenitors had an advantage in becoming activated and internalizing Env compared with bNAb B cell progenitors. We then identified an Env modification strategy that minimized the activation of nNAb B cells targeting epitopes that overlap those of bNAbs.
Wen DC, Noh KM, Goldberg AD, Allis CD, Rosenwaks Z, Rafii S, Banaszynski LA
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Genome Editing a Mouse Locus Encoding a Variant Histone, H3.3B, to Report on its Expression in Live Animals
GENESIS 2014 DEC; 52(12):959-966
Chromatin remodeling via incorporation of histone variants plays a key role in the regulation of embryonic development. The histone variant H3.3 has been associated with a number of early events including formation of the paternal pronucleus upon fertilization. The small number of amino acid differences between H3.3 and its canonical counterparts (H3.1 and H3.2) has limited studies of the developmental significance of H3.3 deposition into chromatin due to difficulties in distinguishing the H3 isoforms. To this end, we used zinc-finger nuclease (ZFN) mediated gene editing to introduce a small C-terminal hemagglutinin (HA) tag to the endogenous H3.3B locus in mouse embryonic stem cells (ESCs), along with an internal ribosome entry site (IRES) and a separately translated fluorescent reporter of expression. This system will allow detection of expression driven by the reporter in cells, animals, and embryos, and will facilitate investigation of differential roles of paternal and maternal H3.3 protein during embryogenesis that would not be possible using variant-specific antibodies. Further, the ability to monitor endogenous H3.3 protein in various cell lineages will enhance our understanding of the dynamics of this histone variant over the course of development. genesis 52:959-966, 2014. (c) 2014 Wiley Periodicals, Inc.