Table 1.

Local immunity modifications in untreated BCC and during therapy with Hh pathway inhibitors.

Untreated BCC
References	Intralesional/TME	Surrounding skin	Notes
Omland et al. (30) and Omland (31)	Increased Tregs	Increased Tregs	Human BCC
	CAFs markers	Intermediated fibroblasts (CAF precursors?)	Human BCC
Kaporis et al. (32)	Th2 dominance (IL4, IL10, CCL2) Increased: - Tregs - Immature dendritic cells Unchanged: CD1b/c+ and CD11c+ Reduced: Langerhans cells (CD1a+)	Increased (slightly) T regs Unchanged CD1b/c+ and CD11c+ Not reduced Langerhans cells (CD1a+)	Human BCC
Grund-Gröschke et al. (40)	Increased Tregs	Not specified	Animal model
	Increased PD1- PDL1 expression
Treated BCC with Hh pathway inhibitors
References (drug)	Intralesional/TME	Surrounding skin	Phase of treatment
Otsuka et al. (42) - Sonidegib (22 pts) - Vismodegib (1 pt)	Upregulated: MHC I Genes for CCL18, CCL21, and CXCL9 Increased: - CD8+ - CD4+ - HLA-DR-class II+mononuclear cells - CD68+ macrophages - VEGF A - T cell -receptor signaling - CD8+/Foxp3+ratio	Increased: - CD8+ - CD4+ - HLA-DR-class II+ mononuclear cells - CD68+ macrophages Not increased: CD8+/Foxp3+ ratio	Regression
Fosko et al. (44) - Vismodegib	Lichenoid dermatitis (immunomediated?)	Not specified	Regression
Miller et al. (43) - Vismodegib	Lack of apoptosis	Not specified	Regression

CAFs, cancer associated fibroblasts; TME, tumor microenvironment; VEGF, vascular endothelial growth factor.