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CD1a promotes systemic manifestations of skin inflammation.
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Dengue virus co-opts innate type 2 pathways to escape early control of viral replication.
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IL-6 effector function of group 2 innate lymphoid cells (ILC2) is NOD2 dependent.
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Multi-Modal Characterization of Monocytes in Idiopathic Pulmonary Fibrosis Reveals a Primed Type I Interferon Immune Phenotype.
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Re-evaluation of human BDCA-2+ DC during acute sterile skin inflammation.
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Resistance to apoptosis underpins the corticosteroid insensitivity of group 2 innate lymphoid cells.
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Proof-of-concept clinical trial of etokimab shows a key role for IL-33 in atopic dermatitis pathogenesis.
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A stromal cell niche sustains ILC2-mediated type-2 conditioning in adipose tissue.
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Fevipiprant, a selective prostaglandin D2 receptor 2 antagonist, inhibits human group 2 innate lymphoid cell aggregation and function.
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Role of NS1 antibodies in the pathogenesis of acute secondary dengue infection.
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Quantification of dengue virus specific T cell responses and correlation with viral load and clinical disease severity in acute dengue infection.
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Cutaneous bacterial sensing through group 2 innate lymphoid cell presentation of endogenous CD1a lipid antigens
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CD1a presentation of endogenous antigens by group 2 innate lymphoid cells.
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Psoriatic T cells recognize neolipid antigens generated by mast cell phospholipase delivered by exosomes and presented by CD1a.
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Filaggrin inhibits house dust mite phospholipase generation of CD1a lipid antigens for recognition by T cells
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Interleukin-33, friend and foe in type-2 immune responses.
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Filaggrin inhibits generation of CD1a neolipid antigens by house dust mite-derived phospholipase
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Jarrett R. et al, (2016), BRITISH JOURNAL OF DERMATOLOGY, 174, E49 - E50
Filaggrin inhibits generation of CD1a neolipid antigens by house dust mite-derived phospholipase.
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