Table 1.
Diseases | NKT type | Subtype | Relativeproportion | Species | Cellular source | Cytokines/Signaling molecules | Functions | References | |
---|---|---|---|---|---|---|---|---|---|
Increase | Decrease | ||||||||
AD | I | CD4- | ↓ | H | PBMC | ‐ | ‐ | ‐ | (10) |
I | DN | ↓ | H | PBMC | ‐ | ‐ | ‐ | (12) | |
I | CD161+ | ↓ | H | PBMC | ‐ | ‐ | ‐ | (13) | |
I | CD4+ | ↑ | H | PBMC | ‐ | ‐ | ‐ | (14) | |
I | DN | ↓ | H | PBMC | IL4 | IFNγ | ‐ | (15) | |
I | ‐ | ↑ | H | PBMC, Skin |
‐ | ‐ | ‐ | (23) | |
I | CXCR4+ | ↑ | H | Skin | ‐ | ‐ | ‐ | (17) | |
I | CXCR4+ | ↑ | M | Skin | IFNγ, IL4, IL17 | ‐ | Pathogenic | (17) | |
I | DN | ↑ | M | Skin | IFNγ, IL2 | ‐ | Protective | (19) | |
I | DN | = | M | Spleen | IL4, IL10 | IFNγ | Pathogenic | (22) | |
ACD | I | ‐ | ↑ | H | Skin | IFNγ, IL4 | ‐ | ‐ | (38) |
I | CD4+, DN |
↑ | M | Spleen | IFNγ | ‐ | ‐ | (39) | |
I | ‐ | ↑ | H | Skin | Perforin, Granzyme B, K | ‐ | ‐ | (41) | |
I | ‐ | ‐ | M | ‐ | IL4, IL13 | ‐ | Protective | (45) | |
I, II | ‐ | ‐ | M | ‐ | ‐ | ‐ | Protective | (46) | |
I | ‐ | ‐ | M | ‐ | ‐ | ‐ | Pathogenic | (51) | |
Psoriasis | I | ‐ | ↓ | H | ‐ | ‐ | ‐ | ‐ | (53) |
I | CD69+ | ↓ | H | PBMC | IL4, IL17, GATA3, RORγt | ‐ | ‐ | (55) | |
I | CD161+ | ↑ | H | Skin | ‐ | ‐ | ‐ | (59) | |
I | ‐ | ↑ | H | Skin | PKCζ | ‐ | ‐ | (61) | |
I | CD161+ | ↑ | H | Skin | IFNγ | ‐ | Pathogenic | (58) | |
UV-induced skin inflammation | I, II | ‐ | ‐ | M | ‐ | ‐ | ‐ | Pathogenic | (66) |
I | ‐ | ‐ | M | Lymph nodes |
IL4 | ‐ | Protective | (67) | |
I | ‐ | ‐ | M | ‐ | ‐ | ‐ | Protective | (68) | |
I, II | ‐ | ‐ | M | ‐ | ‐ | ‐ | Pathogenic | (68) | |
Scleroderma | I | ‐ | ↓ | H | PBMC | IL17 | ‐ | ‐ | (75) |
Alopecia areata |
I | ‐ | ↑ | H | Skin | IL10 | ‐ | Protective | (80) |
Vitiligo | I | CD4+ | ↓ | H | PBMC | ‐ | ‐ | ‐ | (81) |
Skin wound healing | I | ‐ | ‐ | M | ‐ | ‐ | ‐ | Protective | (77–79) |
I, type I; II, type II;‐, not evaluated; DN, double negative; ↑, increase; ↓, decrease; =, no change; H, human; M, mouse; PBMC, peripheral blood mononuclear cells.