An IL-9 fate reporter demonstrates the induction of an innate IL-9 response in lung inflammation

被引：396

作者：

Wilhelm, Christoph ^{[1
]}

Hirota, Keiji ^{[1
]}

Stieglitz, Benjamin ^{[2
]}

Van Snick, Jacques ^{[3
]}

Tolaini, Mauro ^{[1
]}

Lahl, Katharina ^{[4
,5
]}

Sparwasser, Tim ^{[5
]}

Helmby, Helena ^{[6
]}

Stockinger, Brigitta ^{[1
]}

机构：

[1] MRC, Natl Inst Med Res, Div Mol Immunol, Mill Hill, England

[2] MRC, Natl Inst Med Res, Div Mol Struct, Mill Hill, England

[3] Ludwig Inst Canc Res, Brussels, Belgium

[4] Stanford Univ, Dept Pathol, Lab Immunol & Vasc Biol, Sch Med, Stanford, CA 94305 USA

[5] Twincore, Inst Infekt Immunol, Hannover, Germany

[6] London Sch Hyg & Trop Med, London WC1, England

来源：

NATURE IMMUNOLOGY | 2011年 / 12卷 / 11期

基金：

英国医学研究理事会;

关键词：

AIRWAY INFLAMMATION; T-CELLS; MAST-CELLS; EXPRESSION; CYTOKINE; INTERLEUKIN-9; PROMOTES; ANTIBODY; IMMUNITY; ASTHMA;

D O I：

10.1038/ni.2133

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Interleukin 9 (IL-9) is a cytokine linked to lung inflammation, but its cellular origin and function remain unclear. Here we describe a reporter mouse strain designed to map the fate of cells that have activated IL-9. We found that during papain-induced lung inflammation, IL-9 production was largely restricted to innate lymphoid cells (ILCs). IL-9 production by ILCs depended on IL-2 from adaptive immune cells and was rapidly lost in favor of other cytokines, such as IL-13 and IL-5. Blockade of IL-9 production via neutralizing antibodies resulted in much lower expression of IL-13 and IL-5, which suggested that ILCs provide the missing link between the well-established functions of IL-9 in the regulation of type 2 helper T cell cytokines and responses.

引用

页码：1071 / U73

页数：8

共 41 条

[1] Regulation of IL-9 expression by IL-25 signaling [J].

Angkasekwinai, Pornpimon ;

Chang, Seon Hee ;

Thapa, Manoj ;

Watarai, Hiroshi ;

Dong, Chen .

NATURE IMMUNOLOGY, 2010, 11 (03) :250-U9

[2] Induction of an IL7-R+c-Kithi myelolymphoid progenitor critically dependent on IFN-γ signaling during acute malaria [J].

Belyaev, Nikolai N. ;

Brown, Douglas E. ;

Diaz, Ana-Isabel Garcia ;

Rae, Aaron ;

Jarra, William ;

Thompson, Joanne ;

Langhorne, Jean ;

Potocnik, Alexandre J. .

NATURE IMMUNOLOGY, 2010, 11 (06) :477-U41

[3] The transcription factor PU.1 is required for the development of IL-9-producing T cells and allergic inflammation [J].

Chang, Hua-Chen ;

Sehra, Sarita ;

Goswami, Ritobrata ;

Yao, Weiguo ;

Yu, Qing ;

Stritesky, Gretta L. ;

Jabeen, Rukhsana ;

McKinley, Carl ;

Ahyi, Ayele-Nati ;

Han, Ling ;

Nguyen, Evelyn T. ;

Robertson, Michael J. ;

Perumal, Narayanan B. ;

Tepper, Robert S. ;

Nutt, Stephen L. ;

Kaplan, Mark H. .

NATURE IMMUNOLOGY, 2010, 11 (06) :527-U98

[4] Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity [J].

Chang, Ya-Jen ;

Kim, Hye Young ;

Albacker, Lee A. ;

Baumgarth, Nicole ;

McKenzie, Andrew N. J. ;

Smith, Dirk E. ;

DeKruyff, Rosemarie H. ;

Umetsu, Dale T. .

NATURE IMMUNOLOGY, 2011, 12 (07) :631-U186

[5] Anti-interleukin-9 antibody treatment inhibits airway inflammation and hyperreactivity in mouse asthma model [J].

Cheng, G ;

Arima, M ;

Honda, K ;

Hirata, H ;

Eda, F ;

Yoshida, N ;

Fukushima, F ;

Ishii, Y ;

Fukuda, T .

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2002, 166 (03) :409-416

[6] Inhibition of airway remodeling in IL-5-deficient mice [J].

Cho, JY ;

Miller, M ;

Baek, KJ ;

Han, JW ;

Nayar, J ;

Lee, SY ;

McElwain, K ;

McElwain, S ;

Friedman, S ;

Broide, DH .

JOURNAL OF CLINICAL INVESTIGATION, 2004, 113 (04) :551-560

[7] Segmental allergen challenge in patients with atopic asthma leads to increased IL-9 expression in bronchoalveolar lavage fluid lymphocytes [J].

Erpenbeck, VJ ;

Hohlfeld, JM ;

Volkmann, B ;

Hagenberg, A ;

Geldmacher, H ;

Braun, A ;

Krug, N .

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2003, 111 (06) :1319-1327

[8] Identification of an interleukin (IL)-25-dependent cell population that provides IL-4, IL-5, and IL-13 at the onset of helminth expulsion [J].

Fallon, PG ;

Ballantyne, SJ ;

Mangan, NE ;

Barlow, JL ;

Dasvarma, A ;

Hewett, DR ;

McIlgorm, A ;

Jolin, HE ;

McKenzie, ANJ .

JOURNAL OF EXPERIMENTAL MEDICINE, 2006, 203 (04) :1105-1116

[9] Interleukin-9 is involved in host protective immunity to intestinal nematode infection [J].

Faulkner, H ;

Humphreys, N ;

Renauld, JC ;

VanSnick, J ;

Grencis, R .

EUROPEAN JOURNAL OF IMMUNOLOGY, 1997, 27 (10) :2536-2540

[10] Interleukin-9 enhances resistance to the intestinal nematode Trichuris muris [J].

Faulkner, H ;

Renauld, JC ;

Van Snick, J ;

Grencis, RK .

INFECTION AND IMMUNITY, 1998, 66 (08) :3832-3840

← 1 2 3 4 5 →