Table 1.
A selection of recent and important studies implicating each of the innate cell types in the immunopathogenesis of systemic sclerosis (SSc)
| Immune cell | Recent findings | Reference |
|---|---|---|
| T cell | Angiogenic T cells were elevated in SSc patients displaying digital ulcers, which is a severe peripheral vascular complication | 59 |
| Macrophage | The soluble form of the M2 macrophage marker CD163 is elevated in the serum of patients with SSc, highlighting it as a potential biomarker | 66 |
| B cell | Used a mouse model of SSc to demonstrate the importance of B cell homeostasis. Depletion of IL‐6‐producing B effector cells reduced fibrosis while depleting of IL‐10‐producing B regulatory cells had the opposite effect | 97 |
| Mast cell | A subset of SSc patients with localized scleroderma‐like lesions were found to have an inflammatory phenotype leading to the activation of mast cells in the dermis of mechanically stressed skin | 108 |
| Dendritic cell | After depletion of pDCs fibrosis was reverted in mice with established SSc‐like disease. pDC depletion prior to induction of disease also prevented fibrosis | 115 |
| Platelets | Activated platelets induced the production of the profibrotic mediator thymic stromal lymphopoietin (TSLP) in human dermal endothelial cells | 128 |
| Neutrophils | Neutrophil activation was induced by SSc microparticles. Microparticles were derived from platelets and expressed the damage‐associated molecular pattern HMGB1. An inhibitor of HMGB1 attenuated neutrophil activation | 131 |
| Natural killer | A peculiar natural killer cell phenotype in SSc patients was identified characterized by decreased chemokine and activation receptors expression. These SSc‐derived natural killer cells were potent inducers of endothelial microparticle release suggesting that there may be a role for natural killer cells in the activation of endothelial cells in SSc | 133 |
| Innate lymphoid | Type 2 innate lymphoid (ILC2) cells are elevated in patients with SSc. ILC2 counts correlated with skin fibrosis. This study highlights that there may be a profibrotic role for ILC2 cells in SSc | 134 |
| Fibroblast | Although not an immune cell type, fibroblasts exposed to TGF‐β and IL‐17a responded with a 100‐fold increase in the production of IL‐6 | 137 |
DCs = dendritic cells; IL = interleukin; TGF = transforming growth factor; HMGB1 = high mobility group box 1.