Th17 T<sub>EM</sub> cells (expressing <i>IL17A, IL17F, RORC</i>, and <i>STAT3</i>) displayed a higher pathogenic/cytotoxic (<i>IL23R, IL18RAP</i>, and <i>GZMB, CD160, PRF1</i>) gene signature in CD relative to UC, while non-pathogenic/regulatory genes (<i>IL9, FOXP3, CTLA4</i>) were more elevated in UC.
The immunoreactivity for IL-17A, IL-17RA, IL-17E, IL-17RB and IL-17F showed significant decrease in CRC tissue when compared to UC (p = 0.00001. respectively).
Increased IL-17A/IL-17F expression ratio represents the key mucosal T helper/regulatory cell-related gene signature paralleling disease activity in ulcerative colitis.
In general, genes encoding cytokines are genetically polymorphic and polymorphisms in genes IL23R el IL17F were shown associated with susceptibility to Crohn's disease and ulcerative colitis which in their turn are considered as risk factors for developing colorectal cancer (CRC).
Results of the meta-analysis revealed that IL-17A and IL-17F genetic polymorphisms potentially increased UC risk under both allele and dominant models (P < 0.001 for all).
The IL17F (rs763780, 7488T/C) variant was associated with an increased risk for the development of CD, and affected some clinical features of UC and CD.
Our results provided the first evidence that -197A (IL-17A) and 7488T (IL-17F) alleles may influence the susceptibility to and pathophysiological features of UC independently.
The IL17Fp.His161Arg substitution was observed with similar frequencies in IBD patients and controls and was not associated with a certain disease phenotype, but weakly associated with a low body mass index (BMI; P = 0.009) and an earlier age of disease onset (P = 0.039) in UC.