Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

portrait

portrait

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

Recent publications

More publications