Sexual hormones are known to directly modulate immune responses, and, in doing so, alter the development of autoimmune diseases.35 Xenoimmunization of castrated C57BL/6 males and castrated males supplemented with 17β-estradiol resulted in a grade of liver inflammation similar to that observed check details in noncastrated male C57BL/6 mice. Therefore, the absence of

testosterone or the presence of 17β-estradiol in males did not modify the development of AIH. The production of regulatory T cells was also unaffected by the absence of testosterone or presence of 17β-estradiol: castrated males showed significantly more Tregs than females after xenoimmunization. Therefore, in this experimental model of AIH, 17β-estradiol and testosterone levels are not the main factors responsible for the observed sex bias in disease susceptibility. Recently, using Sry(−)Y and Sry(+)X transgenic mice, Smith-Bouvier et al.36 have shown that the XX sex chromosome complement conferred susceptibility to both experimental autoimmune encephalomyelitis and lupus, irrespective of the type of gonads present.36 This observation and our data, although not excluding that sexual hormones could have some influence on the sex bias observed in autoimmune diseases, suggests that other factors related to the X chromosome could be involved in women’s susceptibility

to autoimmune diseases. Selleck AZD1208 In summary, susceptibility to experimental AIH is not influenced by testosterone or estradiol levels nor is it the result of reduced central tolerance. Peripheral tolerance and development of regulatory T cells after self-mimicking antigen exposure are the main factor resulting in susceptibility to AIH. This suggests that the immune response raised to an initiating antigenic event could be the deciding factor for the development

of an AIH. “
“The homeobox gene Barx2 was recently identified as a regulator of ovarian and breast cancer; however, the expression level of BARX2 and its significance in hepatocellular carcinoma (HCC) remain unknown. Protein and mRNA expression levels of Barx2 were examined using Western blotting and real-time PCR respectively, in paired HCC tissue and 上海皓元 matched adjacent non-cancerous tissue from 12 patients. The expression levels of epithelial–mesenchymal transition (EMT) markers were also detected in relation to BARX2 expression. Lastly, immunohistochemistry for BARX2 was also performed on a tissue microarray containing 231 HCC tissue samples. We observed that BARX2 expression was lower in HCC tissues compared to matching adjacent non-cancerous tissue. The low expression level of BARX2 was significantly correlated with metrics of tumor size, tumor differentiation, clinical stage, metastasis and relapse.