Cd209a, also known as SIGNR5 and mouse DC-SIGN (mDC-SIGN), is a C-type lectin receptor (CLR) [1,3,4]. It plays crucial roles in the immune response, particularly in the activation of dendritic cells (DCs) and the regulation of Th17 cell-mediated immune responses. It is involved in signaling pathways related to Raf-1 activation and synergizes with other CLRs like Dectin-2 and Mincle [1,4]. Cd209a is of great biological importance as it is associated with the immunopathology of various diseases. Mouse models are valuable for studying its function in vivo.

In schistosomiasis, CD209a-deficient CBA mice display decreased Th17 responses and are protected from severe immunopathology, indicating that CD209a drives severe Th17 cell-mediated immunopathology [1]. In Helicobacter pylori infection, CD209a mediates LECT2-induced maturation and secretion of DCs, which might hinder the clearance of H. pylori [2]. Also, in murine schistosomiasis, gene silencing in CBA DCs and overexpression in BL/6 DCs demonstrated that CD209a is essential for egg-elicited IL-1β and IL-23 production and subsequent Th17 cell development [3].

In conclusion, Cd209a is a key C-type lectin receptor involved in immune-related signaling pathways, especially in the context of Th17-mediated immunopathology. Gene-knockout mouse models have revealed its significant role in diseases such as schistosomiasis and in the response to H. pylori infection, highlighting its potential as a therapeutic target for these disease areas.