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Andrew C. Issekutz
Researcher at Dalhousie University
Publications - 170
Citations - 11194
Andrew C. Issekutz is an academic researcher from Dalhousie University. The author has contributed to research in topics: Inflammation & Cell adhesion molecule. The author has an hindex of 57, co-authored 170 publications receiving 10699 citations. Previous affiliations of Andrew C. Issekutz include Halifax & University of Buenos Aires.
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Journal ArticleDOI
Pyogenic Bacterial Infections in Humans with MyD88 Deficiency
Horst von Bernuth,Capucine Picard,Capucine Picard,Zhongbo Jin,Rungnapa Pankla,Rungnapa Pankla,Hui Xiao,Cheng-Lung Ku,Cheng-Lung Ku,Maya Chrabieh,Maya Chrabieh,Imen Ben Mustapha,Imen Ben Mustapha,Imen Ben Mustapha,Pegah Ghandil,Pegah Ghandil,Yildiz Camcioglu,Júlia Vasconcelos,Nicolas Sirvent,Margarida Guedes,Artur Bonito Vitor,María José Herrero-Mata,Juan I. Aróstegui,Carlos Rodrigo,Laia Alsina,Estibaliz Ruiz-Ortiz,Manel Juan,Claudia Fortuny,Jordi Yagüe,Jordi Anton,Mariona Pascal,Huey Hsuan Chang,Lucile Janniere,Lucile Janniere,Yoann Rose,Yoann Rose,Ben Zion Garty,Helen Chapel,Andrew C. Issekutz,László Maródi,Carlos Rodríguez-Gallego,Jacques Banchereau,Laurent Abel,Laurent Abel,Xiaoxia Li,Damien Chaussabel,Anne Puel,Anne Puel,Jean-Laurent Casanova,Jean-Laurent Casanova +49 more
TL;DR: Nine children with autosomal recessive MyD88 deficiency suffered from life-threatening, often recurrent pyogenic bacterial infections, including invasive pneumococcal disease, but these patients were otherwise healthy, with normal resistance to other microbes.
Journal ArticleDOI
Selective predisposition to bacterial infections in IRAK-4–deficient children: IRAK-4–dependent TLRs are otherwise redundant in protective immunity
Cheng-Lung Ku,Horst von Bernuth,Horst von Bernuth,Capucine Picard,Shen-Ying Zhang,Huey Hsuan Chang,Kun Yang,Maya Chrabieh,Andrew C. Issekutz,Coleen K. Cunningham,John I. Gallin,Steven M. Holland,Chaim M. Roifman,Stephan Ehl,Joanne Smart,Mimi L.K. Tang,Franck J. Barrat,Ofer Levy,Douglas R. McDonald,Noorbibi K. Day-Good,Richard L. Miller,Hidetoshi Takada,Toshiro Hara,Sami Al-Hajjar,Abdulaziz Al-Ghonaium,David P. Speert,Damien Sanlaville,Xiaoxia Li,Frederic Geissmann,Eric Vivier,László Maródi,Ben Zion Garty,Helen Chapel,Carlos Rodríguez-Gallego,Xavier Bossuyt,Laurent Abel,Anne Puel,Jean-Laurent Casanova +37 more
TL;DR: The IRAK-4–dependent TLRs and IL-1Rs are therefore vital for childhood immunity to pyogenic bacteria, particularly Streptococcus pneumoniae, and appear to play a redundant role in protective immunity to most infections.
Journal ArticleDOI
Clinical Features and Outcome of Patients With IRAK-4 and MyD88 Deficiency
Capucine Picard,Capucine Picard,Horst von Bernuth,Horst von Bernuth,Horst von Bernuth,Pegah Ghandil,Pegah Ghandil,Pegah Ghandil,Maya Chrabieh,Maya Chrabieh,Ofer Levy,Peter D. Arkwright,Douglas R. McDonald,Raif S. Geha,Hidetoshi Takada,Jens C. Krause,C. Buddy Creech,Cheng-Lung Ku,Cheng-Lung Ku,Stephan Ehl,László Maródi,Saleh Al-Muhsen,Saleh Al-Muhsen,Sami Al-Hajjar,Sami Al-Hajjar,Abdulaziz Al-Ghonaium,Abdulaziz Al-Ghonaium,Noorbibi K. Day-Good,Steven M. Holland,John I. Gallin,Helen Chapel,David P. Speert,Carlos Rodríguez-Gallego,Elena Colino,Ben Zion Garty,Chaim M. Roifman,Toshiro Hara,Hideto Yoshikawa,Shigeaki Nonoyama,Joseph B. Domachowske,Andrew C. Issekutz,Mimi L.K. Tang,Joanne Smart,Simona Eva Zitnik,Cyrille Hoarau,Dinakantha S. Kumararatne,Adrian J. Thrasher,E. Graham Davies,Claire Bethune,Nicolas Sirvent,Dominique De Ricaud,Yildiz Camcioglu,Júlia Vasconcelos,Margarida Guedes,Artur Bonito Vitor,Carlos Rodrigo,Francisco Almazán,Maria Méndez,Juan I. Aróstegui,Laia Alsina,Claudia Fortuny,Janine Reichenbach,James W. Verbsky,Xavier Bossuyt,Rainer Döffinger,Laurent Abel,Laurent Abel,Anne Puel,Anne Puel,Jean-Laurent Casanova +69 more
TL;DR: IRAK-4 and MyD88 deficiencies predispose patients to recurrent life-threatening bacterial diseases, such as invasive pneumococcal disease in particular, in infancy and early childhood, with weak signs of inflammation.
Journal ArticleDOI
The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88
Bing He,Raul Santamaria,Weifeng Xu,Montserrat Cols,Kang Chen,Irene Puga,Meimei Shan,Huabao Xiong,James B. Bussel,April Chiu,Anne Puel,Jeanine Reichenbach,László Maródi,Rainer Doffinger,Júlia Vasconcelos,Andrew C. Issekutz,Jens C. Krause,Graham Davies,Xiaoxia Li,Bodo Grimbacher,Alessandro Plebani,Eric Meffre,Capucine Picard,Charlotte Cunningham-Rundles,Jean-Laurent Casanova,Jean-Laurent Casanova,Andrea Cerutti,Andrea Cerutti +27 more
TL;DR: The cytoplasmic domain of TACI encompasses a conserved motif that bound MyD88, an adaptor that activates transcription factor NF-κB signaling pathways via a Toll–interleukin 1 (IL-1) receptor (TIR) domain, which indicates that MyD 88 controls a B cell–intrinsic, TIR-independent, TACi-dependent pathway for immunoglobulin diversification.
Journal ArticleDOI
Hereditary angiodema: a current state-of-the-art review, VII: Canadian Hungarian 2007 International Consensus Algorithm for the Diagnosis, Therapy, and Management of Hereditary Angioedema
Tom Bowen,Marco Cicardi,Konrad Bork,Bruce L. Zuraw,Michael M. Frank,Bruce Ritchie,Henriette Farkas,Lilian Varga,Lorenza C. Zingale,Karen Binkley,Eric Wagner,Peggy Adomaitis,Kristylea Brosz,Jeanne Burnham,Richard Warrington,Chrystyna Kalicinsky,Sean R. Mace,Christine McCusker,R. Robert Schellenberg,Lucia Celeste,Jacques Hébert,Karen A. Valentine,Man-Chiu Poon,Bazir Serushago,Doris Neurath,William H. Yang,Gina Lacuesta,Andrew C. Issekutz,Azza Hamed,Palinder Kamra,John M. Dean,Amin Kanani,Donald Stark,Georges-Etienne Rivard,Eric Leith,Ellie Tsai,Susan Waserman,Paul K. Keith,David Page,Silvia Marchesin,Hilary Longhurst,Wolfhart Kreuz,E. Rusicke,Inmaculada Martinez-Saguer,Emel Aygören-Pürsün,George Harmat,George Füst,Henry Li,Laurence Bouillet,Teresa Caballero,Dumitru Moldovan,Peter J. Späth,Sara Smith-Foltz,István Nagy,Erik Waage Nielsen,Christoph Bucher,Patrik Nordenfelt,Zhi Yu Xiang +57 more
TL;DR: There is a paucity of double-blind, placebo-controlled trials on the treatment of HAE, making levels of evidence to support the algorithm less than optimal.