Gene Primary Function Link to Tregs? Link to Diabetes?
Gzmk[14,16] Induces macrophages to secrete IL-1β (pro-inflammatory IL-1β facilitates conversion of Tregs to Tregs to IL-17 cells No
Cela1 [16] Necessary for differentiation of pancreatic exocrine cells No Signaled downstream of Nkx2.2; Nkx2.2 mutation Nkx2.2; Nkx2.2 mutation death
Clps[19-23] Necessary for efficient dietary lipid & triglyceride hydrolysis Mutations→Fatty Acid disruptions Mutations→increased T2D susceptibility
Pnliprp1 [21] Necessary for efficient triglyceride hydrolysis Mutations→Fatty Acid disruptions Knock-out→increased weight gain & severe insulin resistance (T2D)
Cela2 [16] Linked to pancreatic proelastase II enzyme activity No No
Ctrc[14,16] Linked to trypsinogen activation Trypsinogen hydrolyzes proteins, may play role in Treg function No
Pla2g1b [19-21] Necessary for efficient lipid hydrolysis & fat absorption Mutations→Fatty Acid disruptions can cause Treg membrane alterations & result in cell death Pla2g1b -/- mice are protected from insulin are protected from insulin obesity
Prss1 [14] Linked to trypsinogen activation alterations & result in cell death hydrolyzes proteins, may play role in Treg function No
Table 2: Functional analysis of top 11 preferentially expressed genes: Gene function & location was determined based on intensive literature search of journals & databases (BioGrid & GeneMania). The genes Try5 and Try10 were not included as they are only expressed in Mus musculus, and Ccna2 was not analyzed as its proteins are only expressed in the nucleus.