Table 1.
Global and conditional IL-4Rα gene-deficient mouse models currently available or being characterized.
| Deficient mouse strain | IL-4Rα cell specificity | Reference |
|---|---|---|
| GLOBAL DEFICIENCY | ||
| IL-4Rα−/− | All cells1 | Mohrs et al. (1999) |
| IL-4Rαlox/lox | “Floxed” IL-4Rα | Herbert et al. (2004) |
| CELL-TYPE DEFICIENCY | ||
| LysMcreTgIL-4Rα−/lox | Macrophages and neutrophils2 | Herbert et al. (2004) |
| SMMHCcreTgIL-4Rα−/lox | Smooth muscle cells | Horsnell et al. (2007) |
| LckcreTgIL-4Rα−/lox | CD4+ T lymphocytes3 | Radwanska et al. (2007) |
| iLckcreTgIL-4Rα−/lox | All T lymphocytes4 | Dewals et al. (2009) |
| CD4creTgIL-4Rα−/lox | α/β+ TCR T lymphocytes | Unpublished |
| MB1creTgIL-4Rα−/lox | B lymphocytes5 | Hoving et al. (2012) |
| CD11ccreTgIL-4Rα−/lox | Dendritic cells6 | In characterization |
| LysMcreTgLckcreIL-4Rα−/lox | Macrophages/neutrophils/CD4+/T cells | In characterization |
| INDUCIBLE AND CELL-TYPE DEFICIENCY OR RECONSTITUTION | ||
| TetOIL4RαTg | All cells | Unpublished |
| GT(ROSA)26Sortm1(tTA)Roos/JLysMcre TetOIL4RαTgIL-4Rα−/− | Macrophage/neutrophil reconstitution and inducible deficiency | In characterization |
| LcKtTATg TetOIL4RαTgIL-4Rα−/− | T cell IL-4Rα reconstitution and inducible deficiency | In characterization |
| ERcreTgIL-4Rα−/lox | Inducible global IL-4Rα deficiency | In characterization |
Global IL-4Rα−/− mice1 have revealed a disease exacerbating role for IL-4Rα signaling during primary infection with L. major (Mohrs et al., 1999) and L. mexicana (Alexander et al., 2002) but a protective role during L. donovani infection (Stager et al., 2003a). Furthermore vaccination against L. donovani is ineffective in the absence of IL-4Rα (Stager et al., 2003b). While macrophage/neutrophil specific IL-4Rα−/− mice2 have revealed a significant role for alternative macrophage activation during the course of L. major infection (Hoelscher et al., 2006) no such role was identified following L. mexicana (Bryson et al., 2011) or L. donovani (McFarlane et al., 2011) infection. CD4+ T cell3 and Pan T cell4 specific IL-4Ra−/− mice have identified IL-4Rα signaling through CD4+ T cells as mediating progressive disease following L. major (Radwanska et al., 2007) or L. mexicana (Bryson et al., 2011) infection. Interestingly while CD4+ T cell specific IL-4Rα−/− mice of either sex healed following L. major infection only female mice healed following infection with L. mexicana. Studies are currently ongoing or nearing completion to determine the role of IL-4Rα signaling specifically via B cells5 or DCs6 in these various disease models.