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Article ; Online: Emerging IL-12 family cytokines in the fight against fungal infections.

Thompson, Aiysha / Orr, Selinda J

2018 Volume 111, Page(s) 398–407

Abstract: Invasive fungal infections cause approximately 1.5 million deaths per year worldwide and are a growing threat to human health. Current anti-fungal therapies are often insufficient, therefore studies into host-pathogen interactions are critical for the ... ...

Abstract	Invasive fungal infections cause approximately 1.5 million deaths per year worldwide and are a growing threat to human health. Current anti-fungal therapies are often insufficient, therefore studies into host-pathogen interactions are critical for the development of novel therapies to improve mortality rates. Myeloid cells, such as macrophages and dendritic cells, express pattern recognition receptor (PRRs), which are important for fungal recognition. Engagement of these PRRs by fungal pathogens induces multiple cytokines, which in turn activate T effector responses. Interleukin (IL)-12 family members (IL-12p70, IL-23, IL-27 and IL-35) link innate immunity with the development of adaptive immunity and are also important for regulating T cell responses. IL-12 and IL-23 have established roles during anti-fungal immunity, whereas emerging roles for IL-27 and IL-35 have recently been reported. Here, we discuss the IL-12 family, focusing on IL-27 and IL-35 during anti-fungal immune responses to pathogens such as Candida and Aspergillus.
MeSH term(s)	Adaptive Immunity/immunology ; Animals ; Aspergillus/immunology ; Candida/immunology ; Humans ; Immunity, Innate/immunology ; Interleukin-12/immunology ; Mycoses/immunology ; Signal Transduction/immunology
Chemical Substances	Interleukin-12 (187348-17-0)
Language	English
Publishing date	2018-05-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1018055-2
ISSN	1096-0023 ; 1043-4666
ISSN (online)	1096-0023
ISSN	1043-4666
DOI	10.1016/j.cyto.2018.05.019
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Article ; Online: The Use of Host Biomarkers for the Management of Invasive Fungal Disease.

Griffiths, James S / Orr, Selinda J / Morton, Charles Oliver / Loeffler, Juergen / White, P Lewis

Journal of fungi (Basel, Switzerland)

2022 Volume 8, Issue 12

Abstract: Invasive fungal disease (IFD) causes severe morbidity and mortality, and the number of IFD cases is increasing. Exposure to opportunistic fungal pathogens is inevitable, but not all patients with underlying diseases increasing susceptibility to IFD, ... ...

Abstract	Invasive fungal disease (IFD) causes severe morbidity and mortality, and the number of IFD cases is increasing. Exposure to opportunistic fungal pathogens is inevitable, but not all patients with underlying diseases increasing susceptibility to IFD, develop it. IFD diagnosis currently uses fungal biomarkers and clinical risk/presentation to stratify high-risk patients and classifies them into possible, probable, and proven IFD. However, the fungal species responsible for IFD are highly diverse and present numerous diagnostic challenges, which culminates in the empirical anti-fungal treatment of patients at risk of IFD. Recent studies have focussed on host-derived biomarkers that may mediate IFD risk and can be used to predict, and even identify IFD. The identification of novel host genetic variants, host gene expression changes, and host protein expression (cytokines and chemokines) associated with increased risk of IFD has enhanced our understanding of why only some patients at risk of IFD actually develop disease. Furthermore, these host biomarkers when incorporated into predictive models alongside conventional diagnostic techniques enhance predictive and diagnostic results. Once validated in larger studies, host biomarkers associated with IFD may optimize the clinical management of populations at risk of IFD. This review will summarise the latest developments in the identification of host biomarkers for IFD, their use in predictive modelling and their potential application/usefulness for informing clinical decisions.
Language	English
Publishing date	2022-12-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2784229-0
ISSN	2309-608X ; 2309-608X
ISSN (online)	2309-608X
ISSN	2309-608X
DOI	10.3390/jof8121307
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Article ; Online: Pattern recognition receptors in fungal immunity.

Patin, Emmanuel C / Thompson, Aiysha / Orr, Selinda J

Seminars in cell & developmental biology

2018 Volume 89, Page(s) 24–33

Abstract: Over the last decade, invasive fungal infections have emerged as a growing threat to human health worldwide and novel treatment strategies are urgently needed. In this context, investigations into host-pathogen interactions represent an important and ... ...

Abstract	Over the last decade, invasive fungal infections have emerged as a growing threat to human health worldwide and novel treatment strategies are urgently needed. In this context, investigations into host-pathogen interactions represent an important and promising field of research. Antigen presenting cells such as macrophages and dendritic cells are strategically located at the frontline of defence against potential invaders. Importantly, these cells express germline encoded pattern recognition receptors (PRRs), which sense conserved entities from pathogens and orchestrate innate immune responses. Herein, we review the latest findings regarding the biology and functions of the different classes of PRRs involved in pathogenic fungal recognition. We also discuss recent literature on PRR collaboration/crosstalk and the mechanisms involved in inhibiting/regulating PRR signalling. Finally, we discuss how the accumulated knowledge on PRR biology, especially Dectin-1, has been used for the design of new immunotherapies against fungal infections.
MeSH term(s)	Dendritic Cells/immunology ; Dendritic Cells/microbiology ; Fungi/immunology ; Fungi/pathogenicity ; Germ Cells/immunology ; Germ Cells/microbiology ; Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate/genetics ; Invasive Fungal Infections/genetics ; Invasive Fungal Infections/immunology ; Invasive Fungal Infections/microbiology ; Macrophages/immunology ; Macrophages/microbiology ; Receptors, Pattern Recognition/genetics ; Receptors, Pattern Recognition/immunology
Chemical Substances	Receptors, Pattern Recognition
Language	English
Publishing date	2018-03-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1312473-0
ISSN	1096-3634 ; 1084-9521
ISSN (online)	1096-3634
ISSN	1084-9521
DOI	10.1016/j.semcdb.2018.03.003
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Article: Dependence on Mincle and Dectin-2 Varies With Multiple

Thompson, Aiysha / da Fonseca, Diogo M / Walker, Louise / Griffiths, James S / Taylor, Philip R / Gow, Neil A R / Orr, Selinda J

Frontiers in microbiology

2021 Volume 12, Page(s) 633229

Abstract: More than 95% of ... ...

Abstract	More than 95% of invasive
Language	English
Publishing date	2021-02-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587354-4
ISSN	1664-302X
ISSN	1664-302X
DOI	10.3389/fmicb.2021.633229
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Article ; Online: A Novel Strategy to Identify Haematology Patients at High Risk of Developing Aspergillosis.

Griffiths, James S / White, P Lewis / Thompson, Aiysha / da Fonseca, Diogo M / Pickering, Robert J / Ingram, Wendy / Wilson, Keith / Barnes, Rosemary / Taylor, Philip R / Orr, Selinda J

Frontiers in immunology

2021 Volume 12, Page(s) 780160

Abstract: Invasive Aspergillosis (IA), typically caused by the ... ...

Abstract	Invasive Aspergillosis (IA), typically caused by the fungus
MeSH term(s)	Adult ; Aged ; Aspergillosis/diagnosis ; Aspergillosis/epidemiology ; Aspergillosis/immunology ; Aspergillosis/microbiology ; Aspergillus fumigatus/immunology ; Aspergillus fumigatus/isolation & purification ; Biomarkers, Tumor/blood ; Biomarkers, Tumor/immunology ; Biomarkers, Tumor/metabolism ; Female ; Gene Expression Profiling ; Graft vs Host Disease/immunology ; Graft vs Host Disease/prevention & control ; Hematopoietic Stem Cell Transplantation/adverse effects ; Humans ; Immunocompromised Host ; Immunosuppressive Agents/adverse effects ; Invasive Fungal Infections/diagnosis ; Invasive Fungal Infections/epidemiology ; Invasive Fungal Infections/immunology ; Invasive Fungal Infections/microbiology ; Lectins, C-Type/blood ; Lectins, C-Type/immunology ; Lectins, C-Type/metabolism ; Leukemia, Myeloid, Acute/blood ; Leukemia, Myeloid, Acute/complications ; Leukemia, Myeloid, Acute/immunology ; Leukemia, Myeloid, Acute/therapy ; Male ; Middle Aged ; Polymerase Chain Reaction ; Risk Assessment/methods ; Transplantation, Homologous/adverse effects ; Young Adult
Chemical Substances	Biomarkers, Tumor ; Immunosuppressive Agents ; Lectins, C-Type
Language	English
Publishing date	2021-12-16
Publishing country	Switzerland
Document type	Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.780160
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Article ; Online: Tissue-resident macrophages actively suppress IL-1beta release via a reactive prostanoid/IL-10 pathway.

Ipseiz, Natacha / Pickering, Robert J / Rosas, Marcela / Tyrrell, Victoria J / Davies, Luke C / Orr, Selinda J / Czubala, Magdalena A / Fathalla, Dina / Robertson, Avril Ab / Bryant, Clare E / O'Donnell, Valerie / Taylor, Philip R

The EMBO journal

2020 Volume 39, Issue 14, Page(s) e103454

Abstract: The alarm cytokine interleukin-1β (IL-1β) is a potent activator of the inflammatory cascade following pathogen recognition. IL-1β production typically requires two signals: first, priming by recognition of pathogen-associated molecular patterns leads to ... ...

Abstract	The alarm cytokine interleukin-1β (IL-1β) is a potent activator of the inflammatory cascade following pathogen recognition. IL-1β production typically requires two signals: first, priming by recognition of pathogen-associated molecular patterns leads to the production of immature pro-IL-1β; subsequently, inflammasome activation by a secondary signal allows cleavage and maturation of IL-1β from its pro-form. However, despite the important role of IL-1β in controlling local and systemic inflammation, its overall regulation is still not fully understood. Here we demonstrate that peritoneal tissue-resident macrophages use an active inhibitory pathway, to suppress IL-1β processing, which can otherwise occur in the absence of a second signal. Programming by the transcription factor Gata6 controls the expression of prostacyclin synthase, which is required for prostacyclin production after lipopolysaccharide stimulation and optimal induction of IL-10. In the absence of secondary signal, IL-10 potently inhibits IL-1β processing, providing a previously unrecognized control of IL-1β in tissue-resident macrophages.
MeSH term(s)	Animals ; Epoprostenol/genetics ; Epoprostenol/immunology ; GATA6 Transcription Factor/genetics ; GATA6 Transcription Factor/immunology ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; Interleukin-10/genetics ; Interleukin-10/immunology ; Interleukin-1beta/genetics ; Interleukin-1beta/immunology ; Macrophages, Peritoneal/immunology ; Macrophages, Peritoneal/pathology ; Mice ; Mice, Transgenic
Chemical Substances	GATA6 Transcription Factor ; Gata6 protein, mouse ; IL10 protein, mouse ; IL1B protein, mouse ; Interleukin-1beta ; Interleukin-10 (130068-27-8) ; Epoprostenol (DCR9Z582X0)
Language	English
Publishing date	2020-06-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.15252/embj.2019103454
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Zs.A 1808: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: LAB/NTAL/Lat2: a force to be reckoned with in all leukocytes?

Orr, Selinda J / McVicar, Daniel W

Journal of leukocyte biology

2010 Volume 89, Issue 1, Page(s) 11–19

Abstract: LAB/NTAL/Lat2 is a transmembrane adaptor protein closely related to LAT. It is expressed in various myeloid and lymphoid cells, many of which also express LAT. Phosphorylation of LAB occurs following engagement of various ITAM- and non-ITAM-linked ... ...

Abstract	LAB/NTAL/Lat2 is a transmembrane adaptor protein closely related to LAT. It is expressed in various myeloid and lymphoid cells, many of which also express LAT. Phosphorylation of LAB occurs following engagement of various ITAM- and non-ITAM-linked receptors and can play positive and negative roles following receptor engagement. LAT binds PLCγ directly, resulting in efficient Ca²+ flux and degranulation. However, LAB does not contain a PLCγ-binding motif and only binds PLCγ indirectly, possibly via Grb2, thereby resulting in suboptimal signaling. As LAT can signal more efficiently than LAB, competition between the 2 for space/substrates in the lipid rafts can attenuate signaling. This competition model requires coexpression of LAT; however, LAB is repressive, even in cells lacking substantial LAT expression such as macrophages and mature B cells. The reported interaction between LAB and the ubiquitin E3-ligase c-Cbl suggests 1 possible mechanism for LAT-independent inhibition by LAB, but such a model requires further investigation. Given the wide-reaching expression pattern of LAB, LAB has the ability to modulate signaling in virtually every type of leukocyte. Regardless of its ultimate mode of action, the potent regulatory capability of LAB proves this protein to be a complex adaptor that warrants continued, substantial scrutiny by biochemists and immunologists alike.
MeSH term(s)	Adaptor Proteins, Signal Transducing/chemistry ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Humans ; Leukocytes/metabolism ; Models, Biological ; Protein Binding ; Signal Transduction
Chemical Substances	Adaptor Proteins, Signal Transducing
Language	English
Publishing date	2010-07-19
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.0410221
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Article ; Online: The protective effect of inflammatory monocytes during systemic C. albicans infection is dependent on collaboration between C-type lectin-like receptors.

Thompson, Aiysha / Davies, Luke C / Liao, Chia-Te / da Fonseca, Diogo M / Griffiths, James S / Andrews, Robert / Jones, Adam V / Clement, Mathew / Brown, Gordon D / Humphreys, Ian R / Taylor, Philip R / Orr, Selinda J

PLoS pathogens

2019 Volume 15, Issue 6, Page(s) e1007850

Abstract: Invasive candidiasis, mainly caused by Candida albicans, is a serious healthcare problem with high mortality rates, particularly in immunocompromised patients. Innate immune cells express pathogen recognition receptors (PRRs) including C-type lectin-like ...

Abstract	Invasive candidiasis, mainly caused by Candida albicans, is a serious healthcare problem with high mortality rates, particularly in immunocompromised patients. Innate immune cells express pathogen recognition receptors (PRRs) including C-type lectin-like receptors (CLRs) that bind C. albicans to initiate an immune response. Multiple CLRs including Dectin-1, Dectin-2 and Mincle have been proposed individually to contribute to the immune response to C. albicans. However how these receptors collaborate to clear a fungal infection is unknown. Herein, we used novel multi-CLR knockout (KO) mice to decipher the individual, collaborative and collective roles of Dectin-1, Dectin-2 and Mincle during systemic C. albicans infection. These studies revealed an unappreciated and profound role for CLR co-operation in anti-fungal immunity. The protective effect of multiple CLRs was markedly greater than any single receptor, and was mediated through inflammatory monocytes via recognition and phagocytosis of C. albicans, and production of C. albicans-induced cytokines and chemokines. These CLRs were dispensable for mediating similar responses from neutrophils, likely due to lower expression of these CLRs on neutrophils compared to inflammatory monocytes. Concurrent deletion of Dectin-1 and Dectin-2, or all three CLRs, resulted in dramatically increased susceptibility to systemic C. albicans infection compared to mice lacking a single CLR. Multi-CLR KO mice were unable to control fungal growth due to an inadequate early inflammatory monocyte-mediated response. In response to excessive fungal growth, the multi-CLR KO mice mounted a hyper-inflammatory response, likely leading to multiple organ failure. Thus, these data reveal a critical role for CLR co-operation in the effective control of C. albicans and maintenance of organ function during infection.
MeSH term(s)	Animals ; Candida albicans/immunology ; Candidiasis/genetics ; Candidiasis/immunology ; Chemokines/genetics ; Chemokines/immunology ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; Lectins, C-Type/genetics ; Lectins, C-Type/immunology ; Membrane Proteins/genetics ; Membrane Proteins/immunology ; Mice ; Mice, Knockout ; Monocytes/immunology ; Monocytes/pathology ; Neutrophils/pathology
Chemical Substances	Chemokines ; Clecsf8 protein, mouse ; Lectins, C-Type ; Membrane Proteins ; dectin 1 ; dectin-2, mouse
Language	English
Publishing date	2019-06-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1007850
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Article: Dependence on Dectin-1 Varies With Multiple

Thompson, Aiysha / Griffiths, James S / Walker, Louise / da Fonseca, Diogo M / Lee, Keunsook K / Taylor, Philip R / Gow, Neil A R / Orr, Selinda J

Frontiers in microbiology

2019 Volume 10, Page(s) 1800

Abstract: ... ...

Abstract	Four
Language	English
Publishing date	2019-08-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587354-4
ISSN	1664-302X
ISSN	1664-302X
DOI	10.3389/fmicb.2019.01800
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Article ; Online: A Human Dectin-2 Deficiency Associated With Invasive Aspergillosis.

Griffiths, James S / White, P Lewis / Czubala, Magdalena A / Simonazzi, Elena / Bruno, Mariolina / Thompson, Aiysha / Rizkallah, Pierre J / Gurney, Mark / da Fonseca, Diogo M / Naglik, Julian R / Ingram, Wendy / Wilson, Keith / van de Veerdonk, Frank L / Barnes, Rosemary / Taylor, Philip R / Orr, Selinda J

The Journal of infectious diseases

2020 Volume 224, Issue 7, Page(s) 1219–1224

Abstract: Immunocompromised patients are highly susceptible to invasive aspergillosis. Herein, we identified a homozygous deletion mutation (507 del C) resulting in a frameshift (N170I) and early stop codon in the fungal binding Dectin-2 receptor, in an ... ...

Abstract	Immunocompromised patients are highly susceptible to invasive aspergillosis. Herein, we identified a homozygous deletion mutation (507 del C) resulting in a frameshift (N170I) and early stop codon in the fungal binding Dectin-2 receptor, in an immunocompromised patient. The mutated form of Dectin-2 was weakly expressed, did not form clusters at/near the cell surface and was functionally defective. Peripheral blood mononuclear cells from this patient were unable to mount a cytokine (tumor necrosis factor, interleukin 6) response to Aspergillus fumigatus, and this first identified Dectin-2-deficient patient died of complications of invasive aspergillosis.
MeSH term(s)	Antifungal Agents/therapeutic use ; Aspergillosis/diagnosis ; Aspergillosis/drug therapy ; Aspergillus fumigatus/isolation & purification ; Fatal Outcome ; Host-Pathogen Interactions ; Humans ; Immunocompromised Host ; Invasive Fungal Infections/diagnosis ; Invasive Fungal Infections/drug therapy ; Lectins, C-Type/genetics ; Sequence Deletion/genetics
Chemical Substances	Antifungal Agents ; CLEC6A protein, human ; Lectins, C-Type
Language	English
Publishing date	2020-09-09
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiab145
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