Journal
JOURNAL OF IMMUNOLOGY
Volume 196, Issue 1, Pages 45-54Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1501102
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Funding
- Medical Research Council
- Barrie Trust
- National Institute for Health Research Biomedical Research Centre
- Janssen Pharmaceuticals
- National Institute for Health Research Clinical Research Network
- Asthma UK
- National Institute for Health Research Leicester Respiratory Biomedical Research Unit
- National Institute for Health Research Biomedical Research Centre at Guy's and St. Thomas' National Health Service Foundation Trust
- King's College London
- MRC [G0701693, G116/150, MC_UU_12010/5, MC_U105178805, MC_U137881017] Funding Source: UKRI
- Medical Research Council [G0701693, MC_U105178805, MC_U137881017, G116/150, MC_UU_12010/5] Funding Source: researchfish
- Asthma UK [09/020] Funding Source: researchfish
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Group 2 innate lymphoid cells (ILC2) are important in effector functions for eliciting allergic inflammation, parasite defense, epithelial repair, and lipid homeostasis. ILC2 lack rearranged Ag-specific receptors, and although many soluble factors such as cytokines and lipid mediators can influence ILC2, direct interaction of these cells with the microenvironment and other cells has been less explored. Natural cytotoxicity receptors are expressed by subsets of group 1 ILC and group 3 ILC and thought to be important for their effector function, but they have not been shown to be expressed by ILC2. Therefore, we sought to investigate the expression and functional properties of the natural cytotoxicity receptor NKp30 on human ILC2. A subset of ex vivo and cultured ILC2 express NKp30 that upon interaction with its cognate activatory ligand B7-H6 induces rapid production of type 2 cytokines. This interaction can be blocked by NKp30 blocking Ab and an inhibitory ligand, galectin-3. Higher expression of B7-H6 was observed in lesional skin biopsies of patients with atopic dermatitis, and incubation of keratinocytes with proinflammatory and type 2 cytokines upregulated B7-H6, leading to increased ILC2 cytokine production. NKp30-B7-H6 interaction is a novel cell contact mechanism that mediates activation of ILC2 and identifies a potential target for the development of novel therapeutics for atopic dermatitis and other atopic diseases.
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