Ction, DEXI (dexamethasone-induced transcript) [2,8]. The strongest-known association with T1D maps to popular intronic single nucleotide polymorphisms (SNPs) which can be in higher LD with one another [1,2]. Allelic imbalance studies have demonstrated that the connected SNPs don’t influence CLEC16A transcript expression [1], or that with the surrounding genes (Marchand et al., Zouk et al., unpublished results) in lymphoblastoid cell lines (LCLs). Even so,2013 British Society for Immunology, Clinical and Experimental Immunology, 175: 485H. Zouk et al.other reports show that in the thymus, the T1D-associated intronic SNPs not just influence CLEC16A isoform expression, but also have an effect on the expression of SOCS1 and DEXI [13,14]. Interestingly, an additional current study suggests that intron 19 of CLEC16A, harbouring SNPs most related with T1D along with other AI ailments, may be regulating the expression of DEXI [15]. This tends to make it, additionally to CLEC16A, a possible candidate gene for T1D along with other autoimmune ailments. Formerly generally known as KIAA0350, CLEC16A is really a highly conserved transcript of unknown function which has been classified as a C form lectin as per bioinformatics analysis primarily based on a C form lectin-like domain on exon 14. It is predicted to possess a H4 Receptor Modulator MedChemExpress transmembrane domain (Prosite [16] and Pfam [17]). Nonetheless, it really is believed to not function as a common C kind lectin, whose principal role is recognizing and binding sugars, because it lacks vital domains in carbohydrate recognition [8]. Moreover, the CLEC16A carbohydratebinding website is only 22 amino acids long, as opposed towards the common functionally active C-type lectin domain which is more than 200 amino acids extended [8]. It’s probable that exon 12 may perhaps encode an immunoreceptor tyrosine-based activation motif (ITAM) [8], a function of numerous immune receptors [18]. CLEC16A is expressed preferentially in cells of immune origin, namely B cells, dendritic cells (DCs) and organic killer (NK) cells [19,20], all of that are integral in the pathogenesis of T1D [214]. This strengthens the speculations of CLEC16A’s involvement in immunity, suggesting that it could for that HIV-1 Antagonist custom synthesis reason contribute for the pathogenesis of human AI illnesses, such as T1D. Little is known regarding the function of CLEC16A, its localization, binding partners and mechanism of action. The drosophila orthologue of CLEC16A, Ema, has been located to be an endosomal membrane protein essential for the trafficking of receptor-mediated endocytic cargos [25]. Human CLEC16A expression in drosophila rescues the ema mutant phenotype, suggesting conserved function [25]. CLEC16A, however, could have evolved to play a considerably different function in humans (as observed by its preferential expression in immune cells). Yet another study discovered that CLEC16A was induced in activated rat astrocytes harvested from the inflamed cerebral cortices of rats which have been injected with lipopolysaccharide (LPS), and suggests that it might be involved in the astrocyte-mediated immune response [26]. This outcome merely correlates the presence of CLEC16A with astrocyte inflammation, and requires to be investigated in additional detail. It’s hence clear that further research are expected in order to totally comprehend CLEC16A function and its mechanism of action, ahead of dissecting the extent of its involvement in T1D and other AI ailments. With this in thoughts, we aimed to characterize the function of CLEC16A in B cells. Given that the primary role of antigenpresenting cells (APCs) is antigen presentation and T cell co-st.