Table 1.

Immune cells involved in CSU.

Cell type	The tissue level	Cell activity	Mechanism of activation	Main inflammatory mediators in CSU	References
Mast cells	Increased/Decreased	Activation and degranulation	Autoimmunity (autoantibodies against IgE or FcϵRI-α); dysregulation of the signaling pathways (increased SYK and decreased SHIP); Activation of extrinsic coagulation pathway (increased level of thrombin, D-dimer, FVIIa, F1+2, complement C5a, and TF); physical contact with activated T cells and eosinophils, etc.	Histamine, LTC4, PGD2, tryptase, IL-1β, IL-4, IL-5, IL-8, IL-9, IL-13, IL-31, IL-33, GM-CSF, MMP-9, CXCL1/2, TNFα	(8, 9, 26, 36–38, 48–60)
Basophils	Increased	Activation	Autoimmunity (autoantibodies against IgE or FcϵRI-α); dysregulation of the signaling pathways (increased SYK and decreased SHIP); MCP-1, MBP, IL-3, IL-33, etc.	Histamine, protease, IL-4, IL-6, IL-13, IL-31, IL-33, TNFα, CXCL1	(50, 61–65)
Eosinophils	Increased	Activation	Autoimmunity (autoantibodies against CD23/FCϵRII); physical contact with mast cells; IL-5, TNFα, etc.	MBP, ECP, EPO, TF, VEGF, PAF, MMP-9, IL-6, IL-8, IL-9	(23, 36, 66–69)
T cells	Increased; Decreased frequency of Th17 cells among CD4+ T cells, Decreased frequency of Treg cells among PBMCs (in peripheral blood)	Imbalance of Th1/Th2 cytokines	Imbalance of humoral immunity; physical contact with mast cells; histamine, IL-5, IL-6, IL-18, PGD2, MMP-9, etc.	IL-4, IL-9, IL-10, IL-13, IL-17, IL-23, IL-25, IL-33, TSLP, and TNFα, IFN-λ1	(37, 48, 70–83)
B cells	/	Activation	Autoimmunity	IgE, IgG, IgM, IgA	(14, 19, 84–88)
Macrophages	Increased	Activation	Histamine, IFN-λ1	CXCL1/CXCL2, IL-6, IL-18, IL-33, IFN-λ1	(23, 48, 89–94)
Monocytes	/	Activation	IL-4, IL-8, CXCL8	IL-18, CCL2, MCP-1, CXCL8, TF	(44, 95)
Neutrophils	Increased	Activation	Histamine, IL-1β, IL-8, IL-18, CXCL1/2, CXCL8, GM-CSF	MPO	(23, 25, 48, 90, 96, 97)