Monocytes |
TNF-a |
Classical monocytes in patients with BD can promote TNF-a production and promote Th1 differentiation. |
[1010 Li C, Liu J, Yu X, et al. Aberrant monocyte subsets in patients with Behçet's disease. Clin Immunol. 2021;225:108683.] |
|
sCD14 |
sCD14 increased the adhesion of normal neutrophils to the monolayer of endothelial cells. |
[1212 Sahin S, Lawrence R, Direskeneli H, et al. Monocyte activity in Behçet's disease. Br J Rheumatol. 1996;35(5):424–9.] |
|
TLR2 |
Monocytes may produce neutrophil-stimulated proinflammatory factors through TLR2 that play a role in BD. |
[1414 Neves FS, Carrasco S, Goldenstein-Schainberg C, et al. Neutrophil hyper-chemotaxis in Behçet's disease: a possible role for monocytes orchestrating bacterial-induced innate immune responses. Clin Rheumatol. 2009;28(12):1403–10.] |
|
VEGF, MCP-1 |
VEGF and MCP-1 levels were significantly elevated in BD patients with thrombosis, which promoted the aggregation and adhesion of monocytes. |
[2323 Bozoglu E, Dinc A, Erdem H, et al. Vascular endothelial growth factor and monocyte chemoattractant protein-1 in Behçet's patients with venous thrombosis. Clin Exp Rheumatol. 2005;23(4 Suppl 38):42–S48.] |
|
FcγRIIb, FcγRIII |
Low expression of FcγRIIb and high expression of FcγRIII in monocytes of BD patients may lead to overactivation of BD monocytes. |
[2626 Huang L, Yu X, Li L, et al. Aberrant FcγRIIb and FcγRIII expression on monocytes from patients with Behçet's disease. Clin Immunol. 2020;219:108549.] |
|
CXCL10 |
Post-transcriptional dysregulation of CXCL10 mRNA may lead to an aggravation of BD characteristic inflammatory response. |
[2828 Ambrose N, Khan E, Ravindran R, et al. The exaggerated inflammatory response in Behçet's syndrome: identification of dysfunctional post-transcriptional regulation of the IFN-γ/CXCL10 IP-10 pathway. Clin Exp Immunol. 2015;181(3):427–33.] |
|
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. |
[3030 Castrichini M, Lazzerini PE, Gamberucci A, et al. The purinergic P2×7 receptor is expressed on monocytes in Behçet's disease and is modulated by TNF-α. Eur J Immunol. 2014;44(1):227–38.] |
|
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. |
[3131 Chekaoui A, Belguendouz H, Lahmar K, et al. Uric acid increases IL-1β secretion and Caspase-1 activation in PBMCs of Behçet's disease patients: the in vitro immunomodulatory effect of xanthine oxidase inhibitor Allopurinol. Int Immunopharmacol. 2020;80:106119.] |
Macrophages |
IL-10, CCR1 |
BD-associated CCR1 and IL10 loci can promote polarization of M1 macrophages. |
[3535 Hirahara L, Takase-Minegishi K, Kirino Y, et al. The roles of Monocytes and Macrophages in Behçet's Disease with Focus on M1 and M2 polarization. Front Immunol. 2022;13:852297., 4343 Nakano H, Kirino Y, Takeno M, et al. GWAS-identified CCR1 and IL10 loci contribute to M1 macrophage-predominant inflammation in Behçet's disease. Arthritis Res Ther. 2018;20(1):124.] |
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. |
[8383 Direskeneli H, Fujita H, Akdis CA. Regulation of TH17 and regulatory T cells in patients with Behçet disease. J Allergy Clin Immunol. 2011;128(3):665–6.] |
|
IL-2 |
Treg cells were significantly increased after IL-2 treatment, alleviating the progression of the disease. |
[8787 Liu X, Li W, Liu X, et al. Low-dose IL-2 effectively restored decreased regulatory T cells in patients with Behçet's disease. Clin Exp Rheumatol. 2021;39(4):746–52.] |
|
IL-21 |
IL-21 induced the increase of Th17 cells and the decrease of regulatory Tregs in peripheral blood of BD patients. |
[9090 Geri G, Terrier B, Rosenzwajg M, et al. Critical role of IL-21 in modulating TH17 and regulatory T cells in Behçet disease. J Allergy Clin Immunol. 2011;128(3):655–64.] |
|
INF-α |
The activity of NK cells in peripheral blood of patients with active BD was significantly enhanced after the addition of INF-α. |
[5959 Kaneko F, Takahashi Y, Muramatsu R, et al. Natural killer cell numbers and function in peripheral lymphoid cells in Behcet's disease. Br J Dermatol. 1985;113(3):313–8.] |
NK cells |
IL-17 |
The levels of IL-17 of CD56dim NK cell subset in BD may play a role in neutrophilic infiltration. |
[6161 Gelmez MY, Cinar S, Cetin EA, et al. Inflammatory status might direct ILC and NK cells to IL-17 expressing ILC3 and NK subsets in Behcet's disease. Immunol Lett. 2021;235:1–8.] |
Neutrophils |
sCD40L |
BD patients release higher levels of sCD40L, which promotes neutrophil adhesion and migration. It can also stimulate a burst of neutrophil oxidation |
[5050 Jin R, Yu S, Song Z, et al. Soluble CD40 ligand stimulates CD40-dependent activation of the β2 integrin Mac-1 and protein kinase C zeda (PKCζ) in neutrophils: implications for neutrophil-platelet interactions and neutrophil oxidative burst. PLoS ONE. 2013;8(6):e64631., 5151 Fernández Bello I, Álvarez MT, López-Longo FJ, et al. Platelet soluble CD40L and matrix metalloproteinase 9 activity are proinflammatory mediators in Behçet disease patients. Thromb Haemost. 2012;107(1):88–98., 5454 Perazzio SF, Soeiro-Pereira PV, Dos Santos VC, et al. Soluble CD40L is associated with increased oxidative burst and neutrophil extracellular trap release in Behçet's disease. Arthritis Res Ther. 2017;19(1):235.] |