Clec4n, also known as Dectin-2, is a C-type lectin receptor. It functions as a pattern-recognition receptor for fungi and some components of house dust mite (HDM) extract. It is involved in the activation of signaling pathways such as Syk-NF-κB and Syk-JNK, and plays a role in immune responses, including Th2 and Th17 cell differentiation [1,4].

In Clec4n-deficient (Clec4n(-/-)) mice, HDM-induced allergic airway inflammation was significantly attenuated, with decreased Th2 and Th17 cell differentiation [4]. Also, Clec4n -/- mice had a decreased Th2 immune response following HDM challenge due to reduced type 2 conventional dendritic cells (cDC2s) in the lung [1]. In the context of mycobacterial infection, Clec4n(-/-) mice showed augmented lung pathology as Dectin-2 (Clec4n) contributes to host immunity against mycobacterial infection through the recognition of mannose-capped lipoarabinomannan (Man-LAM) [2]. In a study on epidermolysis bullosa acquisita, although Clec4n was upregulated in lesional skin, deficiency in Clec4n in neutrophil-specific Clec4n -/- mice did not reduce disease in the EBA model [3].

In conclusion, Clec4n, as Dectin-2, is crucial in immune responses, especially in those related to fungal recognition and allergic airway inflammation. Gene-knockout mouse models have been instrumental in revealing its role in these processes, highlighting its potential as a target for treating diseases such as asthma and mycobacterial infections.