Transcriptomics

Dataset Information

3

RORγt+ Innate lymphoid cells transcriptomes after aNKp44 and cytokine stimulation


ABSTRACT: RORγt+ innate lymphoid cells (ILC) are crucial players of innate immune responses and represent a major source of IL-22, which has an important role in mucosal homeostasis. The signals required by RORγt+ ILC to express IL-22 and other cytokines, including TNF, have only partially been elucidated. Here we show that RORγt+ ILC can directly sense the environment by the engagement of the activating receptor NKp44. NKp44 triggering in RORγt+ ILC selectively activates a coordinated pro-inflammatory program, including TNF, while cytokine stimulation induces preferentially IL-22 expression. However, combined engagement of NKp44 and cytokine receptors results in a strong synergistic effect. These data support the concept that NKp44+ RORγt+ ILC can be activated without cytokines and are able to switch between IL-22 or TNF production, depending on the triggering stimulus. Transcriptome analysis of CD56+CD127hi tonsil ILC, Ex vivo and after stimulation with aNKp44, IL-1/IL-7/IL-23 or aNKp44/IL-1/IL-7/IL-23 for 3.5h. RNA was extracted and pooled from 2 donors each, Amplified and labeled according to manufacturer´s instructions (GeneChipU133plus2® , Affymetrix). The analysis was performed in triplicates.

ORGANISM(S): Homo sapiens  

SUBMITTER: Chiara Romagnani   Monica Killig  Johannes Meisig  Timor Glatzer 

PROVIDER: E-GEOD-43409 | ArrayExpress | 2013-10-30

SECONDARY ACCESSION(S): GSE43409PRJNA186006

REPOSITORIES: GEO, ArrayExpress

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Publications


RORγt⁺ innate lymphoid cells (ILCs) are crucial players of innate immune responses and represent a major source of interleukin-22 (IL-22), which has an important role in mucosal homeostasis. The signals required by RORγt⁺ ILCs to express IL-22 and other cytokines have been elucidated only partially. Here we showed that RORγt⁺ ILCs can directly sense the environment by the engagement of the activating receptor NKp44. NKp44 triggering in RORγt⁺ ILCs selectively activated a coordinated proinflammat  ...[more]

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