Functional evaluation of the role of C‐type lectin domain family 16A at the chromosome 16p13 locus

Summary The type 1 diabetes‐associated 16p13 locus contains the CLEC 16 A gene. Its preferential immune cell expression suggests involvement in autoimmunity. Given its elevated expression in dendritic and B cells – known professional antigen‐presenting cells ( APC s) – we hypothesize that C ‐type lectin domain family 16 member A ( CLEC 16 A ) may be involved in T cell co‐stimulation and consequent activation and proliferation. We also sought to identify CLEC 16 A 's subcellular localization. The effect of the CLEC 16 A knock‐down ( KD ) on B cell co‐stimulation and activation of T cells was tested in human lymphoblastoid cell lines ( LCLs ) by co‐culture with CD 4 + T cells. T cell activation and proliferation were determined by flow‐cytometric analysis of CD 69 and CD 25 expression and carboxyfluorescein succinimidyl ester ( CFSE ) dilution, respectively. CLEC 16 A subcellular localization in K 562 cells was examined by immunofluorescence. We show that the CLEC 16 A   KD did not affect the tested indices of lymphoblastoid cell line ( LCL ) APC capacity. Additionally, the percentage of activated T cells following LCL co‐culture was not affected significantly by the CLEC 16 A   KD . T cells co‐cultured with KD or control LCL s also exhibited similar cell division profiles. CLEC 16 A co‐localized with an endoplasmic reticulum ( ER ) marker, suggesting that it may be an ER protein. In conclusion, CLEC 16 A may not be involved in T cell co‐stimulation. Additional studies on CLEC 16 A , accounting for its ER localization, are needed to uncover its biological role.