51 Neither DECR1 nor antibodies
against it have so far been reported to be involved in the pathogenesis of any autoimmune disease. Studies to trace and compare the apoptotic pathway of PDC-E2 and DECR1 may provide more details about the defect of antigen preservation in BECs. Although anti-gp210 and anti-Sp100 are also prominent in patients with PBC, Sp100 was not detected in ABs, CP690550 whereas gp210 was detected in ABs of BrEPCs and HiBECs. Furthermore, our data showed that neither AMA-negative patients with PBC nor any of the control sera reacted with ABs of HiBECs. Thus, the specificity against HiBECs is confined to AMA-positive patients. The role of gp210 and other nuclear antigens in PBC thus still remains unclear. The immunological differences between AMA-positive and AMA-negative patients also remain enigmatic. Interestingly, AMA-negative patients have been detected to have T cell reactivity to the mitochondrial antigens but clearly do not have the same properties against selleckchem ABs as that found in AMA-positive patients. Our study provides additional insights into the apoptosis-related immune tolerance breakdown in PBC. We have obtained data supporting the hypothesis that the incompletely cleaved cellular components specifically generated in biliary epithelium are potential sources of autoantigens
and thus contribute to the formation of PBC. Tolerance to all four MCE公司 identified HiBEC-specific apotopes (PDC-E2, OGDC-E2,
BCOADC-E2, and DECR1) was proved to be broken by the detection of their autoantibodies and/or antigen-specific T cells in PBC.1, 6-8, 52 However, the immunogenicity of each apotope, from 95% for PDC-E2 to 3% for DECR1, shows great diversity, indicating the process is determined by multiple factors that require further investigation. The current results also extend our knowledge about the immunological properties of HiBECs, which indicate that they are more than an innocent victim in the pathogenesis of PBC. A further systematic assessment of the immunobiological features of HiBECs may therefore lead to a better understanding of the biliary-selective damage in PBC. Additional Supporting Information may be found in the online version of this article. “
“We read with interest the article by Suneetha et al. 1 They suggest that hepatitis E virus (HEV)-specific T-cell proliferative responses are decreased in transplant patients, particularly in those with chronic hepatitis. 1 Some important points need to be addressed. The investigators suggest that patients with detectable T-cell responses may not necessarily require antiviral treatment, but might be observed for spontaneous viral clearance. 1 However, they provided insufficient data to support this conclusion. In the transplant resolved-hepatitis group, apart from patient KTxR1, in whom T-cell response was studied during acute infection, very few patients had any T-cell response.