Pyogenic Bacterial Infections in Humans with IRAK-4 Deficiency-Reference-Cited by-同舟云学术

Pyogenic Bacterial Infections in Humans with IRAK-4 Deficiency

Published:2003-03-28 Issue:5615 Volume:299 Page:2076-2079
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Picard Capucine¹,Puel Anne¹,Bonnet Marion¹,Ku Cheng-Lung¹,Bustamante Jacinta¹,Yang Kun¹,Soudais Claire¹,Dupuis Stéphanie¹,Feinberg Jacqueline¹,Fieschi Claire¹,Elbim Carole²,Hitchcock Remi³,Lammas David⁴,Davies Graham⁵,Al-Ghonaium Abdulaziz⁶,Al-Rayes Hassan⁶,Al-Jumaah Sulaiman⁶,Al-Hajjar Sami⁶,Al-Mohsen Ibrahim Zaid⁶,Frayha Husn H.⁶,Rucker Rajivi³,Hawn Thomas R.⁷,Aderem Alan⁷,Tufenkeji Haysam⁶,Haraguchi Soichi³,Day Noorbibi K.³,Good Robert A.³,Gougerot-Pocidalo Marie-Anne²,Ozinsky Adrian⁷,Casanova Jean-Laurent¹⁸

Affiliation:

1. Laboratoire de Génétique Humaine des Maladies Infectieuses, Université René Descartes-INSERM U550, Faculté Necker, 156 rue de Vaugirard, 75015 Paris, France.

2. Service d'Immunologie Cellulaire, Laboratoire d'Hématologie et d'Immunologie, INSERM U294, FacultéXavier Bichat, 75018 Paris, France.

3. Department of Pediatrics, Division of Allergy and Immunology, University of South Florida and All Children's Hospital, St. Petersburg, FL 33701, USA.

4. MRC Center for Immune Regulation, The Medical School, University of Birmingham, Birmingham B15 2TT, UK.

5. Infectious Diseases Unit, Great Ormond Street Hospital for Children, London WC1N 3JH, UK.

6. Department of Pediatrics, King Faisal Specialist Hospital and Research Center, Riyadh 11211, Kingdom of Saudi Arabia.

7. Institute for Systems Biology, 1441 North 34th Street, Seattle, WA 98103, USA.

8. Unitéd'Immunologie et d'Hématologie Pédiatriques, Hôpital Necker-Enfants Malades, 149 rue de Sèvres, 75015 Paris, France.

Abstract

Members of the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) superfamily share an intracytoplasmic Toll–IL-1 receptor (TIR) domain, which mediates recruitment of the interleukin-1 receptor–associated kinase (IRAK) complex via TIR-containing adapter molecules. We describe three unrelated children with inherited IRAK-4 deficiency. Their blood and fibroblast cells did not activate nuclear factor κB and mitogen-activated protein kinase (MAPK) and failed to induce downstream cytokines in response to any of the known ligands of TIR-bearing receptors. The otherwise healthy children developed infections caused by pyogenic bacteria. These findings suggest that, in humans, the TIR-IRAK signaling pathway is crucial for protective immunity against specific bacteria but is redundant against most other microorganisms.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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