Table 3.

The effect of corticosteroids on various steps involved in pathogenesis of dermatophytosis

Immune mediators	Action
Effect on the APCs, neutrophils	1.Glucocorticoids (GCs) act directly on APCs via cytoplasmic/nuclear receptors to suppress the production ofIL-12.
	The inhibition of IL-12 production may represent a major mechanism by which GCs affect the Th1/Th2 balance since IL-12 is the main inducer of Th1 responses, enhancing production Th1 cytokines such as IFN-γ by antigen-primed CD4+ T cells and inhibiting the synthesis of Th2 cytokines such as IL-4 by T cells.
	2. Additionally, exposure of DC to GC induces the expression of TLR2 on their surface and stimulation of these cells with a TLR2 ligand initiates the secretion of IL-10, IL-6, and TNFα, which inhibit Th1 cell activation.
	3. GC have also been shown to decrease the expression of IL-23 in DC, prohibiting Th17 polarization.
	4.GCs may decrease antigen presentation by APCs by decreasing MHC II expression
	5 GCs have been shown to reduce macrophage and neutrophil chemotaxis and decreases the IL-1 and IFN-γ release by macrophages with a small effect on the respiratory burst.
Effect on adaptive immunity (T cells, cytokines)	1.GCs suppress the Th1-cellular immunity axis and mediate a shift towards Th2 immune responses. This results from both a direct effect on T cells by downregulating the expression of IL-12 receptors on T and NK cells leading to a loss of IL-12 responsiveness and indirectly via inhibition of IL-12 production.
	2.GCs have a direct effect on Th2 cells by upregulating the production of IL-4, IL-10, and IL-13
	3.The effects of GC on Th17 cells are unclear; the existing data suggests that both Th17 differentiation and function may be affected by GC. GC administration has been shown to decrease the expression of IL-23 in DC andIL-6, TGFβ as well as IL-17 in the joints of arthritic mice.
	4 In addition to affecting differentiation of specific T-cell subsets, GC directly or indirectly suppress the activation of proinflammatory cytokine genes such as TNFα and IL-1β.

APC: Antigen presenting cell; DC: Dendritic cell; TLR: Toll like receptor; IFN γ: Interferon gamma; NK cell: Natural killer cell; TGFβ: Transforming growth factor beta; TNFα: Tumour necrosis factor alpha