Interplay between C-type lectin receptors and microRNAs in cellular homeostasis and immune response

C-type lectin receptors (CLRs) belong to the family of pattern recognition receptors (PRRs). They have a critical role to play in the regulation of a range of physiological functions including development, respiration, angiogenesis, inflammation, and immunity. CLRs can recognize distinct and conserved exogenous pathogen-associated as well as endogenous damage-associated molecular patterns. These interactions set off downstream signaling cascades, leading to the production of inflammatory mediators, activation of effector immune cells as well as regulation of the developmental and physiological homeostasis. CLR signaling must be tightly controlled to circumvent the excessive inflammatory burden and to maintain the cellular homeostasis. Recently, MicroRNAs (miRNAs) have been shown to be important regulators of expression of CLRs and their downstream signaling. The delicate balance between miRNAs and CLRs seems crucial in almost all aspects of multicellular life. Any dysregulations in the miRNA-CLR axes may lead to tumorigenesis or inflammatory diseases. Here, we present an overview of the current understanding of the central role of miRNAs in the regulation of CLR expression, profoundly impacting upon homeostasis and immunity, and thus, development of therapeutics against immune disorders.

Automated summary

C-type lectin receptors (CLRs) are crucial in regulating physiological functions, recognizing pathogen-associated patterns, and initiating downstream signaling cascades. MicroRNAs (miRNAs) play a key role in regulating CLR expression, and the balance between miRNAs and CLRs is essential in maintaining cellular homeostasis and immunity. Dysregulations in the miRNA-CLR axes may lead to tumorigenesis or inflammatory diseases.