Cells | Cytokines | biological relevance and functional impact | References |
---|---|---|---|
Monocytes | TNF-a | Classical monocytes in patients with BD can promote TNF-a production and promote Th1 differentiation. | [10] |
sCD14 | sCD14 increased the adhesion of normal neutrophils to the monolayer of endothelial cells. | [12] | |
TLR2 | Monocytes may produce neutrophil-stimulated proinflammatory factors through TLR2 that play a role in BD. | [14] | |
VEGF, MCP-1 | VEGF and MCP-1 levels were significantly elevated in BD patients with thrombosis, which promoted the aggregation and adhesion of monocytes. | [23] | |
FcγRIIb, FcγRIII | Low expression of FcγRIIb and high expression of FcγRIII in monocytes of BD patients may lead to overactivation of BD monocytes. | [26] | |
CXCL10 | Post-transcriptional dysregulation of CXCL10 mRNA may lead to an aggravation of BD characteristic inflammatory response. | [28] | |
P2 × 7r | P2 × 7r activation significantly increases IL-1β release from LPS-stimulated BD monocytes, and TNF-α can up-regulate the expression and function of P2 × 7r in monocytes. | [30] | |
UA | Uric acid (UA) can significantly increase the activity levels of NO, IL-1β and caspase-1 in peripheral blood monocytes of BD patients, aggravating the development of BD. | [31] | |
Macrophages | IL-10, CCR1 | BD-associated CCR1 and IL10 loci can promote polarization of M1 macrophages. | |
T cells | IL-17 | Th17 cells can recruit neutrophils to the inflammatory site and mediate the hyperreactivity of BD neutrophils by secreting cytokines such as IL-17. | [83] |
IL-2 | Treg cells were significantly increased after IL-2 treatment, alleviating the progression of the disease. | [87] | |
IL-21 | IL-21 induced the increase of Th17 cells and the decrease of regulatory Tregs in peripheral blood of BD patients. | [90] | |
INF-α | The activity of NK cells in peripheral blood of patients with active BD was significantly enhanced after the addition of INF-α. | [59] | |
NK cells | IL-17 | The levels of IL-17 of CD56dim NK cell subset in BD may play a role in neutrophilic infiltration. | [61] |
Neutrophils | sCD40L | BD patients release higher levels of sCD40L, which promotes neutrophil adhesion and migration. It can also stimulate a burst of neutrophil oxidation |