Table 1.
Molecular and/or cellular deficiencies associated with KO mice and impact on ACAID induction.
| KO molecule | Strain (haplotype) | ACAID is impaired | ACAID is inducible | ||
|---|---|---|---|---|---|
| With cell deficiency | B cells | IgM | B6.129S2-Ighmtm1Cgn/J or C57Bl/6-Igh-6tm1Cgn (H2b) | (15) | |
| (17) | |||||
| T cells | FOXN1 | *Nude (H2d) | (15) | ||
| CD4+ T cells | CD4 | B6.129S2-Cd4tm1Mak (H2b) | (18) | ||
| γδ T cells | TCRδ | C57Bl/6-TCRdtm1 Mom (H2b) | (18) | ||
| (19) | |||||
| (20) | |||||
| NKT/iNKT cells | TCRα | Jα281 or Jα18 KO (H2b or H2d) | (21) | ||
| (22) | |||||
| (23) | |||||
| (24) | |||||
| (25) | |||||
| Without cell deficiency | Soluble molecules | IL-4 | IL-4tmlcgn129 (H2b) | (26) | |
| (15) | |||||
| (27) | |||||
| IL-4 and IL-13 | IL-4−/−/IL-13−/− (H2d) | (24) | |||
| IL-13 | IL-13−/− (H2d) | (24) | |||
| IL-6 | B6,129S2-IL6tmKopf/J (H2b) | (28) | |||
| IL-10 | IL-10tmlcgn129 (H2b) | (15) | |||
| (27) | |||||
| IFNγ | IFNγ−/− (H2b) | (29) | |||
| Plasminogen | Plasminogen KO (H2b) | (25) | |||
| Substance P and neurokinin A | B6.Cg-Tac1tm1Bbm/J (H2b) | (28) | |||
| TSP-1 | TSP1 KO (H2b) | (30) | |||
| Urokinase-type plasminogen activator (uPA) | uPA KO (H2b) | (25) | |||
| Membrane molecules | CD1 | CD1 KO (H-2b) | (31) | ||
| CXCR2 | Cmkar2tm1Mwm (H2d) | (32) | |||
| DR5 | Dr5−/− (H2b) | (33) | |||
| F4/80 | B6.F4/80−/− (H2b) | (34) | |||
| IFNγR | IFNγR−/− (H2b) | (29) | |||
| TGFβRII | **CD4-dnTGFβRII (H2b) | (35) | |||
| TNFRI | TNFRI KO (H2b) | (36) | |||
| TNFRII | TNFRII KO (H2b) | (36) | |||
| TNF-related apoptosis-inducing ligands (TRAIL) | Trail−/− (H2b) | (33) | |||
| uPAR | uPAR KO (H2b) | (25) | |||
| Intracellular molecules | Cbl-b | Cbl-b KO (H2b) | (35) | ||
| STAT6 | STAT6−/− (C129.S2) | (24) | |||
When its gene is knocked, a protein cannot be expressed and a molecular deficiency occurs. In some cases, the lack of a specific protein induces a cell deficiency. Studies of several independent deficiencies have demonstrated the critical nature of the corresponding molecules in anterior chamber-associated immune deviation (ACAID) induction. The table classifies papers studying the ACAID mechanism with knockout (KO) mice according to the phenotypic impact of the KO (with or without cell deficiency). Depending on the molecule deficiency, these papers reported ACAID induction either continued (stated as “ACAID is inducible”) or was inhibited (“ACAID is impaired”).
*Nude mice are not strictly considered KO mice, but are intentionally included because their mutation in the Foxn1 gene induces an absence of mature T cells.
**CD4-TGFβRII mice are not strictly considered KO mice because they overexpress a dominant negative form of TGFβRII, that is, a nonfunctional receptor binding TGFβ with high affinity.
H2b and H2d are the haplotypes of mouse strains used in the referenced studies.