Abstract
BackgroundInnate lymphoid cells (ILC) are part of a heterogeneous family of haematopoietic effector cells which lack re-arranged antigen-specific receptors. They promote host defense and contribute to tissue and metabolic homeostasis, wound healing and immune surveillance. Their role in human cancer immunity is less defined, and therefore we aimed to identify the frequency and phenotype of distinct ILC groups in various types of cancer.MethodsTissue samples and peripheral blood were collected from patients undergoing surgical resection of gastrointestinal and breast tumours. Single cell suspension of tumour tissue was immediately obtained following surgery using tumour dissociation.ResultsWe observed significantly higher frequencies of ILC2 (p value: 0.04) in malignant breast cancer tissue and significantly higher frequencies of group 1 ILC (p value: 0.001) in malignant gastrointestinal tumours. Tumour infiltrating ILC were found to show an activated phenotype with higher expression of MHC-II, KLRG1, early activation marker CD69 and CD44.ConclusionsActivated innate lymphoid cells infiltrate tumours dependent on tumour type and location.
Highlights
Innate lymphoid cells (ILC) are part of a heterogeneous family of haematopoietic effector cells which lack re-arranged antigen-specific receptors
Group 2 ILC are enriched in breast cancer tissue To investigate the potential immune surveillance ability of ILC in breast cancer, we compared the frequency of these cells in malignant and benign tissues
To identify ILC, the single cell suspensions of tumours were stained with common lineage markers (CD3, CD14, CD19, CD11c, CD11b, CD56, IL-3R, FcεRI, TCRαβ and TCRγδ), CD45, CRTH2, IL-7Rα and c-Kit
Summary
Innate lymphoid cells (ILC) are part of a heterogeneous family of haematopoietic effector cells which lack re-arranged antigen-specific receptors. They promote host defense and contribute to tissue and metabolic homeostasis, wound healing and immune surveillance. The importance of adaptive immunity [3] as a key effector cell mechanism in cancer control is well documented. NK cells are not antigen specific and rather identify tumour cells through expression of stress molecules or lack of major histocompatibility complex (MHC-I) receptors ‘missing self’ [8]. Group 1 ILC have cytotoxic abilities and the capacity to produce IFN-γ and TNF-α Their effector function depends on expression of T-bet and Eomes transcription factors. Group 2 ILC are mainly implicated in allergic responses [10, 11] and defence
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