Table 2.

Potential role of MCs in RA pathogenesis and future research agenda

Field	Agenda	Reference
Angiogenesis of RA synovium	Roles of MC origin mediators (such as tryptase, chymase, histamine) on neo-angiogensis of RA synovium	[47,48]
Chemoattractive role in RA synovium	Ability to recruit various immune cells, neutrophil, NK cell, T cell, monocytes via secreting chemokines (TNF-α, CCL2, CCL5, IL-8, LTB4)	[86]
APC function	Activation of other immune cells, such as T cells, via antigen presenting function of MC	[64,65,66,87]
Osteoclastogenesis	Osteoclastogenesis via histamine secreted by MCs	[39,40]
Pharmacologic intervention	c-kit tyrosine kinase inhibitor (imatinib) treatment induced apoptosis of MCs and reduced TNF-α production in RA synovium	[60]
	Anti-allergic medication, tranilast, suppressed TNF-α production in MC of RA mice model	[61]
	MC suppression by salbutamol and cromolyn reduced joint destruction and angiogenesis in RA mice model	[79]

MC, mast cell; RA, rheumatoid arthritis; NK, natural killer; TNF-α, tumor necrosis factor-α; CCL, CC chemokine ligand; IL, interleukin; LTB4, leukotriene B4; APC, antigen presenting cell.