Abstract:
:One of the major obstacles in dissecting the mechanism of pathology in human primary biliary cirrhosis (PBC) has been the absence of animal models. Our laboratory has focused on a model in which mice, following immunization with a xenobiotic chemical mimic of the immunodominant autoepitope of the E2 component of pyruvate dehydrogenase complex (PDC-E2), develop autoimmune cholangitis. In particular, following immunization with 2-octynoic acid (a synthetic chemical mimic of lipoic acid-lysine located within the inner domain of PDC-E2) coupled to bovine serum albumin (BSA), several strains of mice develop typical anti-mitochondrial autoantibodies and portal inflammation. The role of innate immune effector cells, such as natural killer (NK) cells and that NK T cells, was studied in this model based on the hypothesis that early events during immunization play an important role in the breakdown of tolerance. We report herein that, following in-vivo depletion of NK and NK T cells, there is a marked suppression of anti-mitochondrial autoantibodies and cytokine production from autoreactive T cells. However, there was no change in the clinical pathology of portal inflammation compared to controls. These data support the hypothesis that there are probably multiple steps in the natural history of PBC, including a role of NK and NK T cells in initiating the breakdown of tolerance. However, the data suggest that adaptive autoimmune effector mechanisms are required for the progression of clinical disease.
journal_name
Clin Exp Immunoljournal_title
Clinical and experimental immunologyauthors
Shimoda S,Tsuneyama K,Kikuchi K,Harada K,Nakanuma Y,Nakamura M,Ishibashi H,Hisamoto S,Niiro H,Leung PS,Ansari AA,Gershwin ME,Akashi Kdoi
10.1111/j.1365-2249.2012.04581.xsubject
Has Abstractpub_date
2012-06-01 00:00:00pages
279-84issue
3eissn
0009-9104issn
1365-2249journal_volume
168pub_type
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