TABLE 2.
Ion channel expression and function in innate and adaptive immune cells of pancreatic ductal adenocarcinoma.
| Channel | Function | Reference |
|---|---|---|
| Neutrophils | ||
| KCa3.1 | Chemotaxis | Henríquez et al. (2016) |
| Kir2.1 | Possible role in neutrophil proliferation, membrane potential regulation, and Ca2+ influx | Masia et al. (2015) |
| KV1.3 | Membrane potential regulation and electric field detection | Kindzelskii and Petty (2005) |
| TRPC1 | fMLF-stimulated migration and chemotaxis | Lindemann et al. (2015) |
| TRPC6 | Chemotaxis and CXCL1-induced recruitment from the vasculature | Lindemann et al. (2013) and Lindemann et al. (2020) |
| TRPM2 | In vitro transmigration | Yamamoto et al. (2008) |
| P2X7 | IL-1β secretion | Karmakar et al. (2016) |
| HV1 | Ca2+ entry regulation, ROS production, and neutrophil migration | El Chemaly et al. (2010) |
| Ramsey et al. (2009) | ||
| Monocytes/macrophages | ||
| KCa3.1 | M1 polarization | Xu et al. (2017) |
| K2P6.1 | Inflammasome formation | Di et al. (2018) |
| TRPC1 | M1 polarization | Chauhan et al. (2018) |
| TRPM2 | Chemokine production | Yamamoto et al. (2008) |
| TRPM7 | Ca2+-induced macrophage stimulation, proliferation, and M2 polarization | Schilling et al. (2014) and Schappe et al. (2018) |
| HV1 | Phagosomal pH regulation and ROS production | El Chemaly et al. (2014) |
| Dendritic cells | ||
| KV1.3, KV1.5 | MHCII expression, migration, and cytokine production | Matzner et al. (2008) |
| NaV1.7 | Migration | Zsiros et al. (2009) |
| P2X7 | Antigen presentation and migration | Mutini et al. (1999) and Saéz et al. (2017) |
| HV1 | ROS production | Szteyn et al. (2012) |
| Myeloid-derived suppressor cells (MDSCs) | ||
| TRPV1 | Promotes MDSC formation | Hegde et al. (2011) |
| P2X7 | ARG-1, TGF- β1, and ROS up-regulation | Bianchi et al. (2014) |
| NK cells | ||
| KCa3.1 | Negatively influencing proliferation, degranulation, and cytotoxicity | Koshy et al. (2013) |
| KV1.3 | Positively influencing proliferation and degranulation | Koshy et al. (2013) |
| CD4+ and CD8+ T‐cells | ||
| KCa3.1 | Sustaining Ca2+ influx during T-cell activation | Ghanshani et al. (2000) and Wulff et al. (2003) |
| KV1.3 | Sustaining Ca2+ influx during T-cell activation | Wulff et al. (2003) |
| TRPM4 | Motility and cytokine production | Weber et al. (2010) |
| CRAC a | Ca2+ influx during T-cell activation | Feske et al. (2012) |
| Tregs | ||
| KCa3.1 | Still unclear | Estes et al. (2008) |
| KV1.3 | Still unclear | Varga et al. (2009) |
| CRAC b | Development and differentiation | Vaeth et al. (2019) |
| B cells | ||
| KCa3.1 | Sustaining Ca2+ influx during B-cell activation | Wulff et al. (2004) |
| KV1.3 | Sustaining Ca2+ influx during B-cell activation | Wulff et al. (2004) |
| CRAC c | Ca2+ influx during B-cell activation | Feske et al. (2012) |
Murine T‐cells: mRNA and fluorescence-based data indicate that T‐cells up-regulate Orai1 and down-regulate Orai2 when they become activated (Vaeth et al., 2017). The role of Orai3 is controversial (McCarl et al., 2010; Vaeth et al., 2017).
Human peripheral T‐cells: the dominant isoform is Orai1, but all the three genes are up-regulated upon activation (Lioudyno et al., 2008). There is no difference in cell surface expression of ORAI1 between human memory and naive T‐cells (Cox et al., 2013).
Murine peripheral Tregs: mRNA data suggest the expression of Orai1 and Orai2, while much less of Orai3 (Vaeth et al., 2017).
Human peripheral Tregs: ORAI1 and ORAI2, but not ORAI3, were detected using immunocytofluorescence. The expression of Orai1 in Tregs is significantly inferior compared to naive and activated CD4+ T‐cells (Jin et al., 2013).
Murine B cells express Orai1, Orai2 and Orai3 to a comparable extent (Gwack et al., 2008; Vaeth et al., 2017).
Human B cells: no detailed mRNA data. There is no difference in cell surface expression of ORAI1 between memory and naive B cells (Cox et al., 2013).