Clare Hardman
Senior Postdoctoral Scientist
I completed my PhD training at the MRC-Laboratory of Molecular Biology in Cambridge studying the roles of interleukin-33 and group 2 innate lymphoid cells (ILC2) in allergic asthma and type-2 immunity in the group of Dr Andrew McKenzie. My research projects built on the lab’s discovery of ILC2, through investigation of ILC2 activation by IL-33 and effector functions in the lung and during helminth infection. I joined Prof. Graham Ogg’s research group in 2014 as a postdoctoral scientist to continue my investigations of allergy, inflammatory disorders and ILC2, and to extend my experience to human translational research.
My work within the Ogg lab has focussed on the roles of ILC2 in the skin. ILC have typical lymphocyte morphology, originate from the common lymphoid progenitor and mirror the T-helper subsets in transcription factor dependence and cytokine production. Human ILC2 have been identified in the blood, skin, nasal, gut and lung tissue and are principally tissue-resident professional cytokine-producing cells, enriched in number and functional potential in barrier and mucosal tissues. Unlike Th2 cells, ILC2 lack antigen-specific rearranged receptors and are thought to be primarily activated by innate alarmin-like signals. Cutaneous ILC2 are spatially and epigenetically poised to respond to barrier compromise and associated immunological threats. In contrast, CD4+ T cells must undergo significant chromatin remodeling upon activation, highlighting the unique position of ILC2 as sentinels and early effectors mediating responses to cutaneous and mucosal barrier breach. Through analysis of in vivo challenged human skin we identified expression of lipid antigen presentation molecule CD1a on cutaneous ILC2, which was capable of presenting endogenous antigens to T cells. My research builds on the group’s work to understand the cellular and molecular mechanisms underlying skin homeostasis and disease, investigating the therapeutic potential of targeting CD1a pathways in inflammatory skin disorders and to further our knowledge of unconventional lymphocyte populations.
Key publications
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CD1a promotes systemic manifestations of skin inflammation.
Journal article
Hardman CS. et al, (2022), Nat Commun, 13
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IL-6 effector function of group 2 innate lymphoid cells (ILC2) is NOD2 dependent.
Journal article
Hardman CS. et al, (2021), Sci Immunol, 6
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CD1a presentation of endogenous antigens by group 2 innate lymphoid cells.
Journal article
Hardman CS. et al, (2017), Sci Immunol, 2
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Fevipiprant, a selective prostaglandin D2 receptor 2 antagonist, inhibits human group 2 innate lymphoid cell aggregation and function.
Journal article
Hardman C. et al, (2019), J Allergy Clin Immunol, 143, 2329 - 2333
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IL‐33 citrine reporter mice reveal the temporal and spatial expression of IL‐33 during allergic lung inflammation
Journal article
Hardman CS. et al, (2013), European Journal of Immunology, 43, 488 - 498
Recent publications
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Group A Streptococcus induces CD1a-autoreactive T cells and promotes psoriatic inflammation.
Journal article
Chen Y-L. et al, (2023), Sci Immunol, 8
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CD1a promotes systemic manifestations of skin inflammation.
Journal article
Hardman CS. et al, (2022), Nat Commun, 13
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Dengue virus co-opts innate type 2 pathways to escape early control of viral replication.
Journal article
Fonseka CL. et al, (2022), Commun Biol, 5
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IL-6 effector function of group 2 innate lymphoid cells (ILC2) is NOD2 dependent.
Journal article
Hardman CS. et al, (2021), Sci Immunol, 6
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Multi-Modal Characterization of Monocytes in Idiopathic Pulmonary Fibrosis Reveals a Primed Type I Interferon Immune Phenotype.
Journal article
Fraser E. et al, (2021), Front Immunol, 12