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Article ; Online: Androgen receptor signaling promotes Treg suppressive function during allergic airway inflammation

Vivek D. Gandhi / Jacqueline-Yvonne Cephus / Allison E. Norlander / Nowrin U. Chowdhury / Jian Zhang / Zachary J. Ceneviva / Elie Tannous / Vasiliy V. Polosukhin / Nathan D. Putz / Nancy Wickersham / Amrit Singh / Lorraine B. Ware / Julie A. Bastarache / Ciara M. Shaver / Hong Wei Chu / R. Stokes Peebles Jr. / Dawn C. Newcomb

The Journal of Clinical Investigation, Vol 132, Iss

2022 Volume 4

Abstract: Women have higher prevalence of asthma compared with men. In asthma, allergic airway inflammation is initiated by IL-33 signaling through ST2, leading to increased IL-4, IL-5, and IL-13 production and eosinophil infiltration. Foxp3+ Tregs suppress and ... ...

Abstract	Women have higher prevalence of asthma compared with men. In asthma, allergic airway inflammation is initiated by IL-33 signaling through ST2, leading to increased IL-4, IL-5, and IL-13 production and eosinophil infiltration. Foxp3+ Tregs suppress and ST2+ Tregs promote allergic airway inflammation. Clinical studies showed that the androgen dehydroepiandrosterone (DHEA) reduced asthma symptoms in patients, and mouse studies showed that androgen receptor (AR) signaling decreased allergic airway inflammation. Yet the impact of AR signaling on lung Tregs remains unclear. Using AR-deficient and Foxp3 fate-mapping mice, we determined that AR signaling increased Treg suppression during Alternaria extract (Alt Ext; allergen) challenge by stabilizing Foxp3+ Tregs and limiting the number of ST2+ ex-Tregs and IL-13+ Th2 cells and ex-Tregs. AR signaling also decreased Alt Ext–induced ST2+ Tregs in mice by limiting expression of Gata2, a transcription factor for ST2, and by decreasing Alt Ext–induced IL-33 production from murine airway epithelial cells. We confirmed our findings in human cells where 5α-dihydrotestosterone (DHT), an androgen, decreased IL-33–induced ST2 expression in lung Tregs and decreased Alt Ext–induced IL-33 secretion in human bronchial epithelial cells. Our findings showed that AR signaling stabilized Treg suppressive function, providing a mechanism for the sex difference in asthma.
Keywords	Inflammation ; Pulmonology ; Medicine ; R
Subject code	610
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	American Society for Clinical Investigation
Document type	Article ; Online
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Article: Th17-mediated inflammation in asthma

Newcomb, Dawn C / Peebles, R Stokes, Jr

Current Opinion in Immunology. 2013 Dec., v. 25, no. 6

2013

Abstract: Asthma is a heterogeneous disease with many different phenotypes. Moderate and severe asthma phenotypes have been associated with increased neutrophils and increased Th17 cytokines, IL-17A, IL-17F, and IL-22, in the bronchoalveolar lavage fluid of ... ...

Abstract	Asthma is a heterogeneous disease with many different phenotypes. Moderate and severe asthma phenotypes have been associated with increased neutrophils and increased Th17 cytokines, IL-17A, IL-17F, and IL-22, in the bronchoalveolar lavage fluid of patients. Th17 cytokines recruit neutrophils to the airway by increasing secretion of epithelial-derived neutrophilic chemokines. In addition, Th17 cytokines also induce mucous cell metaplasia and have pleotropic effects on airway smooth muscle resulting in airway narrowing. The role of Th17 cytokines in regulating Th2 cytokine expression and allergic airway inflammation remains unclear with conflicting reports. However, the role of Th17 cells in asthma will be answered in ongoing clinical trials with therapeutics targeting IL-17A and IL-17 receptor signaling.
Keywords	asthma ; chemokines ; clinical trials ; inflammation ; interleukin-17 ; metaplasia ; neutrophils ; patients ; phenotype ; secretion ; smooth muscle ; therapeutics
Language	English
Dates of publication	2013-12
Size	p. 755-760.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2013.08.002
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Article ; Online: Selective Pharmaceutical Inhibition of PARP14 Mitigates Allergen-Induced IgE and Mucus Overproduction in a Mouse Model of Pulmonary Allergic Response.

Eddie, Alex M / Chen, Kevin W / Schenkel, Laurie B / Swinger, Kerren K / Molina, Jennifer R / Kunii, Kaiko / Raybuck, Ariel L / Keilhack, Heike / Gibson-Corley, Katherine N / Niepel, Mario / Peebles, R Stokes / Boothby, Mark R / Cho, Sung Hoon

ImmunoHorizons

2022 Volume 6, Issue 7, Page(s) 432–446

Abstract: The type 2 cytokines IL-4 and IL-13, which share use of an IL-4 receptor α-chain and its nuclear induction of the transcription factor STAT6, are crucial in elicitation and maintenance of allergic conditions including asthma. STAT6 binds poly(ADP-ribose) ...

Abstract	The type 2 cytokines IL-4 and IL-13, which share use of an IL-4 receptor α-chain and its nuclear induction of the transcription factor STAT6, are crucial in elicitation and maintenance of allergic conditions including asthma. STAT6 binds poly(ADP-ribose) polymerase (PARP)14, an ADP-ribosyl monotransferase. Elimination of PARP14 by gene targeting led to attenuation of OVA-specific allergic lung inflammation. However, PARP14 has multiple functional domains apart from the portion that catalyzes ADP-ribosylation, and it is not clear whether inhibition of the catalytic function has any biological consequence. Using BALB/c mice sensitized to the allergen
MeSH term(s)	Allergens ; Animals ; Asthma/drug therapy ; Disease Models, Animal ; Immunoglobulin E ; Mice ; Mucus/metabolism ; Pharmaceutical Preparations/metabolism ; Poly(ADP-ribose) Polymerase Inhibitors/metabolism ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Poly(ADP-ribose) Polymerase Inhibitors/therapeutic use ; Poly(ADP-ribose) Polymerases/genetics ; Poly(ADP-ribose) Polymerases/metabolism ; Poly(ADP-ribose) Polymerases/therapeutic use
Chemical Substances	Allergens ; Pharmaceutical Preparations ; Poly(ADP-ribose) Polymerase Inhibitors ; Immunoglobulin E (37341-29-0) ; Parp14 protein, mouse (EC 2.4.2.30) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30)
Language	English
Publishing date	2022-07-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2573-7732
ISSN (online)	2573-7732
DOI	10.4049/immunohorizons.2100107
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Article: Response to infections in patients with asthma and atopic disease: An epiphenomenon or reflection of host susceptibility?

James, Kristina M / Peebles, R. Stokes, Jr / Hartert, Tina V

The Journal of Allergy and Clinical Immunology. 2012 Aug., v. 130, no. 2

2012

Abstract: Associations between respiratory tract infections and asthma inception and exacerbations are well established. Infant respiratory syncytial virus and rhinovirus infections are known to be associated with an increased risk of asthma development, and among ...

Abstract	Associations between respiratory tract infections and asthma inception and exacerbations are well established. Infant respiratory syncytial virus and rhinovirus infections are known to be associated with an increased risk of asthma development, and among children with prevalent asthma, 85% of asthma exacerbations are associated with viral infections. However, the exact nature of this relationship remains unclear. Is the increase in severity of infections an epiphenomenon, meaning respiratory tract infections just appear to be more severe in patients with underlying respiratory disease, or instead a reflection of altered host susceptibility among persons with asthma and atopic disease? The main focus of this review is to summarize the available levels of evidence supporting or refuting the notion that patients with asthma or atopic disease have an altered susceptibility to selected pathogens, as well as discussing the biological mechanism or mechanisms that might explain such associations. Finally, we will outline areas in need of further research because understanding the relationships between infections and asthma has important implications for asthma prevention and treatment, including potential new pathways that might target the host immune response to select pathogens.
Keywords	asthma ; children ; immune response ; pathogens ; patients ; people ; risk ; viruses ; covid19
Language	English
Dates of publication	2012-08
Size	p. 343-351.
Publishing place	Mosby, Inc.
Document type	Article
ZDB-ID	121011-7
ISSN	1085-8725 ; 1097-6825 ; 0091-6749
ISSN (online)	1085-8725 ; 1097-6825
ISSN	0091-6749
DOI	10.1016/j.jaci.2012.05.056
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Article: PGI2 as a regulator of CD4+ subset differentiation and function

Boswell, Madison G / Zhou, Weisong / Newcomb, Dawn C / Peebles, R. Stokes, Jr

PROSTAGLANDINS & OTHER LIPID MEDIATORS. 2011 Nov., v. 96, no. 1-4

2011

Abstract: Prostaglandin (PG)I2 has important regulatory functions on the innate and adaptive immune systems. Recent experimental evidence reveals that PGI2 modulates the development and function of CD4+ T cells subsets, including Th1, Th2, and Th17 cell responses. ...

Abstract	Prostaglandin (PG)I2 has important regulatory functions on the innate and adaptive immune systems. Recent experimental evidence reveals that PGI2 modulates the development and function of CD4+ T cells subsets, including Th1, Th2, and Th17 cell responses. In vitro and in vivo studies support that PGI2 generally has an inhibitory effect on Th1 and Th2 activation, differentiation, and cytokine production. In contrast, PGI2 seems to enhance Th17-favoring polarization conditions, resulting in Th17 cytokine production. Therefore, PGI2 may either promote or inhibit individual CD4+ cell subsets and impact adaptive immune responses.
Keywords	CD4-positive T-lymphocytes ; adaptive immunity ; cytokines ; in vivo studies ; iodine ; prostaglandins
Language	English
Dates of publication	2011-11
Size	p. 21-26.
Publishing place	Elsevier Inc.
Document type	Article
ISSN	1098-8823
DOI	10.1016/j.prostaglandins.2011.08.003
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Article ; Online: Testosterone Attenuates Group 2 Innate Lymphoid Cell-Mediated Airway Inflammation

Jacqueline-Yvonne Cephus / Matthew T. Stier / Hubaida Fuseini / Jeffrey A. Yung / Shinji Toki / Melissa H. Bloodworth / Weisong Zhou / Kasia Goleniewska / Jian Zhang / Sarah L. Garon / Robert G. Hamilton / Vasiliy V. Poloshukin / Kelli L. Boyd / R. Stokes Peebles, Jr. / Dawn C. Newcomb

Cell Reports, Vol 21, Iss 9, Pp 2487-

2017 Volume 2499

Abstract: Sex hormones regulate many autoimmune and inflammatory diseases, including asthma. As adults, asthma prevalence is 2-fold greater in women compared to men. The number of group 2 innate lymphoid cells (ILC2) is increased in patients with asthma, and we ... ...

Abstract	Sex hormones regulate many autoimmune and inflammatory diseases, including asthma. As adults, asthma prevalence is 2-fold greater in women compared to men. The number of group 2 innate lymphoid cells (ILC2) is increased in patients with asthma, and we investigate how testosterone attenuates ILC2 function. In patients with moderate to severe asthma, we determine that women have an increased number of circulating ILC2 compared to men. ILC2 from adult female mice have increased IL-2-mediated ILC2 proliferation versus ILC2 from adult male mice, as well as pre-pubescent females and males. Further, 5α-dihydrotestosterone, a hormone downstream of testosterone, decreases lung ILC2 numbers and IL-5 and IL-13 expression from ILC2. In vivo, testosterone attenuated Alternaria-extract-induced IL-5+ and IL-13+ ILC2 numbers and lung eosinophils by intrinsically decreasing lung ILC2 numbers, as well as by decreasing expression of IL-33 and thymic stromal lymphopoietin (TSLP), ILC2-stimulating cytokines. Collectively, these findings provide a foundational understanding of sexual dimorphism in ILC2 function.
Keywords	innate lymphoid cells ; testosterone ; sex hormones ; asthma ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2017-11-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Group 2 Innate Lymphoid Cells Coordinate Damage Response in the Stomach.

Meyer, Anne R / Engevik, Amy C / Madorsky, Toni / Belmont, Erika / Stier, Matthew T / Norlander, Allison E / Pilkinton, Mark A / McDonnell, Wyatt J / Weis, Jared A / Jang, Bogun / Mallal, Simon A / Peebles, R Stokes / Goldenring, James R

Gastroenterology

2020 Volume 159, Issue 6, Page(s) 2077–2091.e8

Abstract: Background & aims: Severe injury to the lining of the stomach leads to changes in the epithelium (reprogramming) that protect and promote repair of the tissue, including development of spasmolytic polypeptide-expressing metaplasia (SPEM) and tuft and ... ...

Abstract	Background & aims: Severe injury to the lining of the stomach leads to changes in the epithelium (reprogramming) that protect and promote repair of the tissue, including development of spasmolytic polypeptide-expressing metaplasia (SPEM) and tuft and foveolar cell hyperplasia. Acute gastric damage elicits a type-2 inflammatory response that includes production of type-2 cytokines and infiltration by eosinophils and alternatively activated macrophages. Stomachs of mice that lack interleukin 33 (IL33) or interleukin 13 (IL13) did not undergo epithelial reprogramming after drug-induced injury. We investigated the role of group 2 innate lymphoid cells (ILC2s) in gastric epithelial repair. Methods: Acute gastric injury was induced in C57BL/6J mice (wild-type and RAG1 knockout) by administration of L635. We isolated ILC2s by flow cytometry from stomachs of mice that were and were not given L635 and performed single-cell RNA sequencing. ILC2s were depleted from wild-type and RAG1-knockout mice by administration of anti-CD90.2. We assessed gastric cell lineages, markers of metaplasia, inflammation, and proliferation. Gastric tissue microarrays from patients with gastric adenocarcinoma were analyzed by immunostaining. Results: There was a significant increase in the number of GATA3-positive ILC2s in stomach tissues from wild-type mice after L635-induced damage, but not in stomach tissues from IL33-knockout mice. We characterized a marker signature of gastric mucosal ILC2s and identified a transcription profile of metaplasia-associated ILC2s, which included changes in expression of Il5, Il13, Csf2, Pd1, and Ramp3; these changes were validated by quantitative polymerase chain reaction and immunocytochemistry. Depletion of ILC2s from mice blocked development of metaplasia after L635-induced injury in wild-type and RAG1-knockout mice and prevented foveolar and tuft cell hyperplasia and infiltration or activation of macrophages after injury. Numbers of ILC2s were increased in stomach tissues from patients with SPEM compared with patients with normal corpus mucosa. Conclusions: In analyses of stomach tissues from mice with gastric tissue damage and patients with SPEM, we found evidence of type 2 inflammation and increased numbers of ILC2s. Our results suggest that ILC2s coordinate the metaplastic response to severe gastric injury.
MeSH term(s)	Animals ; Disease Models, Animal ; Gastric Mucosa/drug effects ; Gastric Mucosa/immunology ; Gastric Mucosa/pathology ; Humans ; Immunity, Innate ; Interleukin-33/genetics ; Lymphocyte Subsets/immunology ; Metaplasia/chemically induced ; Metaplasia/genetics ; Metaplasia/immunology ; Mice ; Mice, Knockout
Chemical Substances	Il33 protein, mouse ; Interleukin-33
Language	English
Publishing date	2020-09-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2020.08.051
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Article ; Online: A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach.

Petersen, Christine P / Meyer, Anne R / De Salvo, Carlo / Choi, Eunyoung / Schlegel, Cameron / Petersen, Alec / Engevik, Amy C / Prasad, Nripesh / Levy, Shawn E / Peebles, R Stokes / Pizarro, Theresa T / Goldenring, James R

Gut

2017 Volume 67, Issue 5, Page(s) 805–817

Abstract: Objective: Alternatively activated macrophages (M2) are associated with the progression of spasmolytic polypeptide-expressing metaplasia (SPEM) in the stomach. However, the precise mechanism(s) and critical mediators that induce SPEM are unknown.: ... ...

Abstract	Objective: Alternatively activated macrophages (M2) are associated with the progression of spasmolytic polypeptide-expressing metaplasia (SPEM) in the stomach. However, the precise mechanism(s) and critical mediators that induce SPEM are unknown. Design: To determine candidate genes important in these processes, macrophages from the stomach corpus of mice with SPEM (DMP-777-treated) or advanced SPEM (L635-treated) were isolated and RNA sequenced. Effects on metaplasia development after acute parietal cell loss induced by L635 were evaluated in interleukin (IL)-33, IL-33 receptor (ST2) and IL-13 knockout (KO) mice. Results: Profiling of metaplasia-associated macrophages in the stomach identified an M2a-polarised macrophage population. Expression of IL-33 was significantly upregulated in macrophages associated with advanced SPEM. L635 induced metaplasia in the stomachs of wild-type mice, but not in the stomachs of IL-33 and ST2 KO mice. While IL-5 and IL-9 were not required for metaplasia induction, IL-13 KO mice did not develop metaplasia in response to L635. Administration of IL-13 to ST2 KO mice re-established the induction of metaplasia following acute parietal cell loss. Conclusions: Metaplasia induction and macrophage polarisation after parietal cell loss is coordinated through a cytokine signalling network of IL-33 and IL-13, linking a combined response to injury by both intrinsic mucosal mechanisms and infiltrating M2 macrophages.
MeSH term(s)	Animals ; Flow Cytometry ; Gastric Mucosa/metabolism ; Immunohistochemistry ; Interleukin-13/genetics ; Interleukin-13/metabolism ; Interleukin-33/metabolism ; Macrophages/metabolism ; Metaplasia/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Parietal Cells, Gastric/cytology ; Peptides/metabolism ; Real-Time Polymerase Chain Reaction ; Receptors, Interleukin/genetics ; Signal Transduction ; Stomach/cytology
Chemical Substances	Il1rl1 protein, mouse ; Interleukin-13 ; Interleukin-33 ; Peptides ; Receptors, Interleukin ; spasmolytic polypeptide
Language	English
Publishing date	2017-02-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80128-8
ISSN	1468-3288 ; 0017-5749
ISSN (online)	1468-3288
ISSN	0017-5749
DOI	10.1136/gutjnl-2016-312779
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Article: Human TH17 cells express a functional IL-13 receptor and IL-13 attenuates IL-17A production

Newcomb, Dawn C / Boswell, Madison G / Zhou, Weisong / Huckabee, Matthew M / Goleniewska, Kasia / Sevin, Carla M / Khurana Hershey, Gurjit K / Kolls, Jay K / Peebles, R. Stokes, Jr

The Journal of Allergy and Clinical Immunology. 2011 Apr., v. 127, no. 4

2011

Abstract: BACKGROUND: IL-13 is a central mediator of airway responsiveness and mucus expression in patients with allergic airway inflammation, and IL-13 is currently a therapeutic target for asthma. However, little is known about how IL-13 regulates human CD4+ T- ... ...

Abstract	BACKGROUND: IL-13 is a central mediator of airway responsiveness and mucus expression in patients with allergic airway inflammation, and IL-13 is currently a therapeutic target for asthma. However, little is known about how IL-13 regulates human CD4+ T-cell lineages because IL-13 receptor (IL-13R) α1, a subunit of IL-13R, has not previously been reported to exist on human T cells. OBJECTIVE: We sought to determine whether human CD4+ TH17 cells express IL-13Rα1 and whether IL-13 regulates TH17 cytokine production. METHODS: Naive human CD4+ cells were isolated from whole blood, activated with anti-CD3 and anti-CD28, and polarized to TH1, TH2, TH17, or induced regulatory T cells in the presence of IL-13 (0-10 ng/mL). Cell supernatants, total RNA, or total protein was examined 4 days after TH17 polarization. RESULTS: TH17 cells, but not TH0, TH1, TH2, or induced regulatory T cells, expressed IL-13Rα1. IL-13 attenuated IL-17A production, as well as expression of retinoic acid–related orphan receptor, runt-related transcription factor-1, and interferon regulatory factor 4 in TH17-polarized cells. IL-13 neither inhibited IFN-γ production from TH1 cells nor inhibited IL-4 production from TH2 cells. Furthermore, attenuation of IL-17A production only occurred when IL-13 was present within 24 hours of T-cell activation or at the time of restimulation. CONCLUSIONS: IL-13Rα1 is expressed on human CD4+ TH17 cells, and IL-13 attenuates IL-17A production at polarization and restimulation. Although IL-13 is an attractive therapeutic target for decreasing symptoms associated with asthma, these results suggest that therapies inhibiting IL-13 production could have adverse side effects by increasing IL-17A production.
Keywords	CD4-positive T-lymphocytes ; RNA ; adverse effects ; asthma ; humans ; inflammation ; interferon regulatory factor-4 ; interferon-gamma ; interleukin-13 ; interleukin-17 ; interleukin-4 ; mucus ; patients
Language	English
Dates of publication	2011-04
Size	p. 1006-1013.e4.
Publishing place	Mosby, Inc.
Document type	Article
ZDB-ID	121011-7
ISSN	1085-8725 ; 1097-6825 ; 0091-6749
ISSN (online)	1085-8725 ; 1097-6825
ISSN	0091-6749
DOI	10.1016/j.jaci.2010.11.043
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Article: Conditional regulation of cyclooxygenase-2 in tracheobronchial epithelial cells modulates pulmonary immunity

Park, G.Y / Hu, N / Wang, X / Sadikot, R.T / Yull, F.E / Joo, M / Stokes Peebles, R. Jr / Blackwell, T.S / Christman, J.W

Clinical and experimental immunology. 2007 Nov., v. 150, no. 2

2007

Abstract: Cyclooxygenase-2 (COX-2) gene expression in the lung is induced in pathological conditions such as asthma and pneumonia; however, the exact impact of COX-2 gene expression in the airway in regulating inflammatory and immunological response in the lung is ...

Abstract	Cyclooxygenase-2 (COX-2) gene expression in the lung is induced in pathological conditions such as asthma and pneumonia; however, the exact impact of COX-2 gene expression in the airway in regulating inflammatory and immunological response in the lung is not understood. To define a physiological role of inducible COX-2 in airway epithelial cells, we developed a novel line of transgenic mice, referred to as CycloOxygenase-2 TransActivated (COTA) mice, that overexpress a COX-2 transgene in the distribution of the CC-10 promoter in response to doxycycline. In response to doxycycline treatment, COX-2 expression was increased in airway epithelium of COTA mice and whole lung tissue contained a three- to sevenfold increase in prostaglandin E₂ (PGE₂), prostaglandin D₂ (PGD₂) thromboxane B₂ (TXB₂) and 6-Keto prostaglandin F₂α (PGF₂α) compared to wild-type and untreated COTA mice. Interestingly, primary mouse tracheal epithelial cells from COTA mice produced only PGE₂ by doxycycline-induced COX-2 activation, providing an indication of cellular specificity in terms of mediator production. In the ovalbumin model, in which doxycycline was given at the sensitization stage, there was an increase in interleukin (IL)-4 level in lung tissue from COTA mice compared to untreated COTA and wild-type mice. In addition, COTA mice that were treated with doxycycline had impaired clearance of Pseudomonas aeruginosa pneumonia compared to wild-type mice. COX-2 gene expression in airway epithelial cells has an important role in determining immunological response to infectious and allergic agents.
Keywords	asthma ; Pseudomonas aeruginosa
Language	English
Dates of publication	2007-11
Size	p. 245-254.
Publisher	Blackwell Publishing Ltd
Publishing place	Oxford, UK
Document type	Article
ZDB-ID	218531-3
ISSN	1365-2249 ; 0009-9104 ; 0964-2536
ISSN (online)	1365-2249
ISSN	0009-9104 ; 0964-2536
DOI	10.1111/j.1365-2249.2007.03478.x
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