*The Relationship between microRNAs, ILC2s and Th2 Cells DOI: http://dx.doi.org/10.5772/intechopen.107450*

the Th1/Th2 ratio and hypersecretion of Th2 cytokines are currently thought pivotal in the pathogenesis of allergic asthma. Cells that produce Th2-type cytokines include type 2 helper T cells (Th2), follicular helper T cells (TFH), basophils, mast cells, and type 2 innate lymphoid-like cells (ILC2s). ILC2s and Th2 cells can induce type 2 immunopathology by releasing type 2 effector cytokines [66]. As a result, ILC2s offer a primary source of early intrinsic cells driving the classical type 2 cytokines in eosinophilic inflammation. Participating as regulators of immunity by coordinating multiple target genes in multiple cells, MiRNAs can modulate Th2 cell differentiation, Th1/Th2 balance, and promote type 2 immune responses, and thus participate in the development and progression of asthma. ILC2s are critical initiators of allergic inflammation. They all participate in asthma onset and development. Many miRNAs mentioned above are involved in Th2 cell responses and ILC2s reactions, contributing to more or less the development of allergic diseases. Priti, who compared the miRNAs transcriptomes of ILC2s and Th2 cells in lung tissue, concluded that miRNAs expression is necessary to maintain ILC2 homeostasis *in vivo*, which can be mediated by participating in the regulation of overlapping but not identical target genes of innate and adaptive immune cells to achieve certain expected biological outcomes that can contribute to the development of allergic disease [51]. Therefore, we might also consider that specific miRNAs affect both Th2 and ILC2s through common pathways, exacerbating or contributing to certain allergic diseases, such as asthma. A common link between MicroRNAs, ILC2s, and Th2 remains to be further investigated.
