. 2020 Sep 25;11:565275. doi: 10.3389/fimmu.2020.565275

TABLE 2.

Functions of ILLs in inflammatory arthritis.

Subtypes	Subsets and distribution (Human)	Functions and mechanism (Mice)	References
NKT	(1) IFN-γ⁺NKT in SF of RA; (2) RORγt⁺T-bet^lowPLZF^– iNKT with Th17-like response in joints of PsA and other SpA.	(1) IL-17⁺ NKT promote murine arthritis; (2) CD1d-dependent NKT protect murine arthritis by dampening Th1 cell responses; (1) Dampening combined gut and joint inflammation in SpA.	(55–64)
MAIT	(1) MAIT with IL-17 phenotype in SF of RA; (2) CD8⁺IL-17⁺IL-23R⁺ MAIT in SF of PsA; (3) CD8⁺IL-17⁺IL-23R⁺IL-7R⁺ MAIT in SF of SpA.	(1) MAIT exacerbate in murine CIA model; (2) IL-23/IL-17 axis in MAIT contribute to PsA; (3) IL-7/IL-17 axis in MAIT contribute to AS and other SpA.	(66–71)
γδ17 T	(1) CCR5⁺CXCR3⁺ IL-17-producing Vδ2 T in RA; (2) TEM Vγ9⁺Vδ2⁺ IL-17-producing T cells with HLA-DR and CD86 expression in SF of RA; (3) TEMγδ17 T cells in peripheral and synovium of PsA; (4) IL-23R⁺RORγt⁺ γδ17 T cells in active AS and other SpA.	(1) In CIA murine arthritis, IL-17 producing Vγ4⁺ γδ T promoted disease development; (2) In Il1rn^–/– spontaneously developed arthritis, CCR2⁺Vγ6⁺ γδ17 T cells participate in disease progression.	(29, 62, 78–84)
Innate-like B	(1) Reduced B10 cells in PBMC of RA; (2) Impaired B10 cells in PBMC and SF of PsA; (3) CD19⁺CD24^hiCD38^hi B10 cells decreased in PBMC and SF of SpA	(1) CII-reactive MZB cells exhibit spontaneous IgM and significant APC capacity for murine arthritis development; (2) B10 is crucial for suppression of Th1/Th17 response and induction of T regulatory type 1 cells; (3) B10 directly inhibit Th17 cells generation via reduction of STAT3 phosphorylation and RORγt expression; (1) B10 present CD1d-lipid and induced iNKT cells to secrete IFN-γ to ameliorate arthritis.	(89–99)