Ulcers

Ulcers / 2010 / Article / Tab 1

Review Article

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.

FactorsObserved effectsReferences

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-blockersBeta-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 smokingIFN-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 deficiencyTLR2-induced anti-inflammatory responses (↑IL-10)[42]