Table 1.
Summary of the role of innate immune cells in the pathogenesis and progression of axSpA
| Immune cell population | Role in axSpA | Reference |
|---|---|---|
| Macrophages | Active sacroiliitis shows predominant cellular infiltration with macrophages | 64 |
| CD163+ macrophages and CD68+ macrophages from fibrous tissue of axSpA facet joints secrete IL-23 | 85 | |
| Normal enthesis harbours a population of CD14+ cells capable of IL-23 and TNF production | 55 | |
| Dendritic cells | Impaired formation of conjugates between dendritic cells and T cells due to impaired accessory molecule function | 65 |
| Defects in co-stimulation, decreased expression of MHC II and altered cytoskeletal dynamics in axSpA patients | 66, 86, 87 | |
| NK cells | HLA-B27 heavy chain homodimers and heterodimers bind and activate NK cells through killer cell immunoglobulin like receptor | 68, 69 |
| High NK cell cytotoxicity in SpA patients compared with controls | 88 | |
| Lower expression of A20, responsible for NF-κB inhibition on CD56bright cells in patients with axSpA | 89 | |
| MICA serves as a ligand to NKG2D and the complex results in the activation of effector cytolytic function of NKG2D-expressing cells against MICA-expressing cells | 71 | |
| Invariant NK T cells | iNKT depletion worsened joint inflammation in TNF AU-rich regulatory element mouse model | 73 |
| iNKT cells secrete IL-17 upon stimulation of the TCR or IL-23R | 72 | |
| γδ T cells | γδ T cells population has been shown to be the predominant IL-17A producers at the enthesis in the IL-23-dependent mouse model | 4 |
| γδ T cells are resident in the enthesis and express transcripts associated with the IL-23–IL-17 pathway, including RORC, CCR6 and IL-23R | 58 | |
| γδ T cells has been shown to drive IL-17 secretion independent of IL-23 stimulation | 58 | |
| γδ T were enriched within inflamed joints of SpA and acts as a major IL-17 secretors | 90 | |
| Innate lymphoid cells | ILC3 groups are relevant to SpA due to secretion of IL-17 and IL-22 in response to activation by IL-23 | 77 |
| Gut-derived ILC3 were expanded in the synovial fluid and bone marrow of patients with axSpA | 77 | |
| Normal enthesis harbours a population of resident ILC3 | 79 | |
| Psoriatic arthritis is characterized by a skewed ILC homeostasis, with elevated levels of ILC3s, which are potent source of IL-17/IL-22 | 91 | |
| MAIT | Enriched population in the synovial fluid of patients with axSpA | 16 |
| Secretion of IL-17 independent of IL-23. Role in IL-22 secretion and regulation of bone formation | 82 | |
| The number of IL-22+ and IFN-γ+/IL-17A+ MAIT cells was higher in axSpA as compared with healthy controls | 82 |