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Table 1 Regulation of related cytokines in BD

From: The roles of immune cells in Behçet’s disease

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.

[35, 43]

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

[50, 51, 54]