Possible Association between Th1 Immune Polarization and Epithelial Permeability with Toll-Like Receptors 2 Dysfunction in the Pathogenesis of the Recurrent Aphthous Ulceration

Table 1

Th1 polarization induced by factors associated with RAU.

Factors	Observed effects	References
Th1 polarization of immune response in the RAU	↑ IL-2, IL-12, IFN-γ, and ↓ IL-4	[16]
	↑ TH1/TH2 diverse genes (microarray)	[10]
	↓HSP27 and ↓ IL-10	[17]
	↑ IFN-γ, TNF-α, IL-2, IL-4, IL-5, and ↓ IL-10	[18]
	↑ IFN-γ, TNF-α, IL-2, IL-5, IL-6, IL-8 and ↓ IL-10, and TGF-β and ↓ CD4^+CD25^+	[19]
Stress	↑ IL-1, IL-6, IL-8, IL-18, and TNF-α	[20]
	↑ IFN-γ, TNF-α IL-6, IL-10, and IL-5	[21]
	↑ IFN-γ, IL-2 and ↓IL-10, and IL-4	[22]
	↓ inhibitory effect of catecholamines on IFN-γ and failure to shift to Th2 responses	[23]
NSAIDs	↑TNF-α	[24]
	↑ IFN-γ, TNF-α, IL-2 and ↓ IL-4, and IL-6	[25]
Bromelain	↑ TNF-α and IFN-γ	[26]
	↑ permeability of the mucosa	[27]
Beta-blockers	Beta-blockers cause Th1 polarization	[28]
Imiquimod (TLR7)	↑ IFN-γ, IL-12, IL-6, and TNF-α	[29]
Hypovitaminosis	↓ B12 = ↑ TNF-α and ↓of EGF	[30]
	↓ B6 = ↑ TNF-α	[31]
Cigarette smoking	IFN-γ/IL-10 (Th1/Th2) ratio is lower in smokers	[32]
	↓IL-12 p40/IL-10 ratio	[33]
	↓ IL-2 and TNF-α	[34]
Pregnancy	↑Th2/Th1 cytokines ratio	[35]
Breatfeeding	↑regulatory T cells	[36]
Thalidomide	↓ TNF-α, ↓IL-12 and ↑IL-10 (LPS stimulation)	[37, 38]
TNF inhibitors	↓ TNF-α and ↑CD4^+CD25^+in situ (Infliximab)	[39]
	↓ CD4^+CD25^+ spontaneous apoptosis (Infliximab)	[40]
	↓ TNF-α, IL-2 and IFN-γ (pentoxifylline)	[41]
TLR2 deficiency	TLR2-induced anti-inflammatory responses (↑IL-10)	[42]