Immunity to infection in IL-17-deficient mice and humans

被引:141
作者
Cypowyj, Sophie [1 ]
Picard, Capucine [2 ,3 ,4 ]
Marodi, Laszlo [5 ]
Casanova, Jean-Laurent [1 ,2 ,4 ,6 ]
Puel, Anne [2 ]
机构
[1] Rockefeller Univ, St Giles Lab Human Genet Infect Dis, Rockefeller Branch, New York, NY 10021 USA
[2] Univ Paris 05, Lab Human Genet Infect Dis, Necker Branch, Necker Med Sch,INSERM,U980, Paris, France
[3] Hop Necker Enfants Malad, AP HP, Study Ctr Primary Immunodeficiencies, Paris, France
[4] Paris Descartes Univ, Fac Med Necker, Paris, France
[5] Univ Debrecen, Dept Infect & Pediat Immunol, Med & Hlth Sci Ctr, H-4012 Debrecen, Hungary
[6] Hop Necker Enfants Malad, AP HP, Pediat Immunohematol Unit, Paris, France
基金
美国国家卫生研究院;
关键词
Cytokines; IL-17; Infectious diseases; CHRONIC MUCOCUTANEOUS CANDIDIASIS; CD4(+) T-CELLS; HOST-DEFENSE; TH17; CELLS; INBORN-ERRORS; IFN-GAMMA; BACTERIAL-INFECTION; GENETIC DISSECTION; STAT1; DEFICIENCY; MURINE MODEL;
D O I
10.1002/eji.201242605
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Mice with defective IL-17 immunity display a broad vulnerability to various infectious agents at diverse mucocutaneous surfaces. In humans, the study of patients with various primary immunodeficiencies, including autosomal dominant hyper-IgE syndrome caused by dominant-negative STAT3 mutations and autosomal recessive autoimmune polyendocrinopathy syndrome type 1 caused by null mutations in AIRE, has suggested that IL-17A, IL-17F and/or IL-22 are essential for mucocutaneous immunity to Candida albicans. This hypothesis was confirmed by the identification of rare patients with chronic mucocutaneous candidiasis (CMC) due to autosomal recessive IL-17RA deficiency and autosomal dominant IL-17F deficiency. Heterozygosity for gain-of-function mutations in STAT1 in additional patients with CMC was recently shown to inhibit the development of IL-17 T cells. Although the infectious phenotype of patients with CMC and inborn errors of IL-17 immunity remains to be finely delineated, it appears that human IL-17A and IL-17F display redundancy for protective immunity in natural conditions that is not seen in their mouse orthologs in experimental conditions.
引用
收藏
页码:2246 / 2254
页数:9
相关论文
共 123 条
[1]   The phenotype of human STK4 deficiency [J].
Abdollahpour, Hengameh ;
Appaswamy, Giridharan ;
Kotlarz, Daniel ;
Diestelhorst, Jana ;
Beier, Rita ;
Schaeffer, Alejandro A. ;
Gertz, E. Michael ;
Schambach, Axel ;
Kreipe, Hans H. ;
Pfeifer, Dietmar ;
Engelhardt, Karin R. ;
Rezaei, Nima ;
Grimbacher, Bodo ;
Lohrmann, Sabine ;
Sherkat, Roya ;
Klein, Christoph .
BLOOD, 2012, 119 (15) :3450-3457
[2]   Primary immunodefciency diseases: an update on the classification from the International Union of Immunological Societies Expert Committee for Priary Immunodeficiency [J].
Al-Herz, Waleed ;
Bousfiha, Aziz ;
Casanova, Jean-Laurent ;
Chapel, Helen ;
Conley, Mary Ellen ;
Cunningham-Rundles, Charlotte ;
Etzioni, Amos ;
Fischer, Alain ;
Luis Franco, Jose ;
Geha, Raif S. ;
Hammarstrom, Lennart ;
Nonoyama, Shigeaki ;
Notarangelo, Luigi Daniele ;
Ochs, Hans Dieter ;
Puck, Jennifer M. ;
Roifman, Chaim M. ;
Seger, Reinhard ;
Tang, Mimi L. K. .
FRONTIERS IN IMMUNOLOGY, 2011, 2
[3]   Life-threatening infectious diseases of childhood: single-gene inborn errors of immunity? [J].
Alcais, Alexandre ;
Quintana-Murci, Lluis ;
Thaler, David S. ;
Schurr, Erwin ;
Abel, Laurent ;
Casanova, Jean-Laurent .
YEAR IN HUMAN AND MEDICAL GENETICS: NEW TRENDS IN MENDELIAN GENETICS, 2010, 1214 :18-33
[4]   Human genetics of infectious diseases: between proof of principle and paradigm [J].
Alcais, Alexandre ;
Abel, Laurent ;
Casanova, Jean-Laurent .
JOURNAL OF CLINICAL INVESTIGATION, 2009, 119 (09) :2506-2514
[5]   Regulation of Gastric B Cell Recruitment Is Dependent on IL-17 Receptor A Signaling in a Model of Chronic Bacterial Infection [J].
Algood, Holly M. Scott ;
Allen, Shannon Sedberry ;
Washington, Mary K. ;
Peek, Richard M., Jr. ;
Miller, Geraldine G. ;
Cover, Timothy L. .
JOURNAL OF IMMUNOLOGY, 2009, 183 (09) :5837-5846
[6]   TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1 [J].
Amadi-Obi, Ahjoku ;
Yu, Cheng-Rong ;
Liu, Xuebin ;
Mahdi, Rashid M. ;
Clarke, Grace Levy ;
Nussenblatt, Robert B. ;
Gery, Igal ;
Lee, Yun Sang ;
Egwuagu, Charles E. .
NATURE MEDICINE, 2007, 13 (06) :711-718
[7]   THE CLINICAL SPECTRUM OF PATIENTS WITH DEFICIENCY OF SIGNAL TRANSDUCER AND ACTIVATOR OF TRANSCRIPTION-1 [J].
Averbuch, Diana ;
Chapgier, Ariane ;
Boisson-Dupuis, Stephanie ;
Casanova, Jean-Laurent ;
Engelhard, Dan .
PEDIATRIC INFECTIOUS DISEASE JOURNAL, 2011, 30 (04) :352-355
[8]  
Bader O, 2012, CLIN INFECT DIS, V54, P1035, DOI 10.1093/cid/cir943
[9]   Interleukin 27 limits autoimmune encephalomyelitis by suppressing the development of interleukin 17-producing T cells [J].
Batten, Marcel ;
Li, Ji ;
Yi, Sothy ;
Kljavin, Noelyn M. ;
Danilenko, Dimitry M. ;
Lucas, Sophie ;
Lee, James ;
de Sauvage, Frederic J. ;
Ghilardi, Nico .
NATURE IMMUNOLOGY, 2006, 7 (09) :929-936
[10]   Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells [J].
Bettelli, E ;
Carrier, YJ ;
Gao, WD ;
Korn, T ;
Strom, TB ;
Oukka, M ;
Weiner, HL ;
Kuchroo, VK .
NATURE, 2006, 441 (7090) :235-238