Abstract
Myeloid C-type lectin receptors (CLRs) are important sensors of self and non-self that work in concert with other pattern recognition receptors (PRRs). CLRs have been previously classified based on their signaling motifs as activating or inhibitory receptors. However, specific features of the ligand binding process may result in distinct signaling through a single motif, resulting in the triggering of non-canonical pathways. In addition, CLR ligands are frequently exposed in complex structures that simultaneously bind different CLRs and other PRRs, which lead to integration of heterologous signaling among diverse receptors. Herein, we will review how sensing by myeloid CLRs and crosstalk with heterologous receptors is modulated by many factors affecting their signaling and resulting in differential outcomes for immunity and inflammation. Finding common features among those flexible responses initiated by diverse CLR-ligand partners will help to harness CLR function in immunity and inflammation.
Highlights
Myeloid C-type lectin receptors (CLRs) are important sensors of self and non-self that work in concert with other pattern recognition receptors (PRRs)
We will review how sensing by myeloid CLRs and crosstalk with heterologous receptors is modulated by many factors affecting their signaling and resulting in differential outcomes for immunity and inflammation
This study suggests that DCIR acts as an activating receptor for the STAT1-type I IFN signaling, and speculates that DCIR may function as a molecular sink binding unphosphorylated inactive Src homology region domain-containing phosphatase (SHP)-2, limiting SHP-2′s capacity to deactivate STAT1
Summary
While signaling motifs allow to predict effector responses following sensing by CLRs, this canonical response is subjected to modulation by the physical nature, affinity, and avidity of the ligand [2]. Based on their intracellular signaling motifs, myeloid CLRs can be classified into the following broad categories (Figure 1): immunoreceptor tyrosine-based activating motif (ITAM)-coupled CLRs, hemi-ITAM-(hemITAM)-bearing CLRs, immunoreceptor tyrosine-based inhibitory motif (ITIM)-containing CLRs, and a group of CLRs lacking typical signaling motifs [1, 3, 4].
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