Table 2.

Th-dependent diseases. IFN = interferon; IL = interleukin; TNF = tumour necrosis factor; CNS = central nervous system; Treg = T regulatory cells; PD = Parkinson’s disease.

	Evidence for Th Polarisation	Ref.
Th1
Atherosclerosis	CD4+ T-cells dominate atherosclerotic plaques. Increase IFN-γ and IL-2, IL-12, IL-18.	[70]
Rheumatoid arthritis	Increase in IFN-γ+CD4+ T-cells in peripheral blood and IFN-γ and TNF-α expression. Reduction in IL-6 and IL10 expression.	[105]
Type I diabetes	High IFN-γ expression drives persistent signal in pancreatic beta cells.	[106]
Multiple sclerosis	IFN-γ-producing Th1 cells most frequent Th cell subset in the CNS.	[107]
Parkinson’s	PD patients more Th1 cells and fewer Treg cells. CD4+ T-cells mediate brain inflammation.	[108] [109]
Th2
Asthma	Production of Th2 cytokines IL-4, IL-13, IL-5, increased production of IgE by B-cells. Genes that enhanced Th2 polarisation (IL17RB) and Th2 cytokine (IL-25) production were upregulated in asthma.	[110] [111]
Ulcerative colitis	Overexpression of Bcl2L12 by CD4+ T-cells upregulates Th2 responses and downregulates Th2 ell apoptosis.	[112]
Chronic fatigue syndrome	Shift from Th1 to Th2 profile correlated with illness parameters including increase in IL-4 and reduced natural killer cell cytotoxicity.	[113]