Abstract
Although the autoimmune regulator (Aire) knockout (KO) mouse model has been reported to present various organ-specific autoimmune diseases depending on genetic background, autoimmune pancreatitis in mice of BALB/c background has not yet been reported. Here, we report that Aire KO mice with BALB/cAnN background showed significant lymphoid cell infiltration in the pancreas and stomach. To examine whether the phenotype in the pancreas and stomach is due to autoimmune reaction associated with autoantibody production, indirect immunofluorescence staining followed by Western blot analysis was performed. Consequently, the autoantibody against pancreas and stomach was detected in the sera of Aire KO mice, and the target antigen of the autoantibody was identified as protein disulfide isomerase-associated 2 (Pdia2), which was reported to be expressed preferentially in the pancreas and stomach. Thus, Aire KO mice of BALB/cAnN background can serve as a useful animal model for autoimmune gastro-pancreatitis with anti-Pdia2 autoantibody production.
Highlights
Autoimmunity is caused by failure of immunological tolerance for self-tissue antigen
autoimmune regulator (Aire) KO and wild type (WT) mice were examined under a microscope
It is well known that Aire deficiency leads to an autoimmne reaction directed against a wide spectrum of various organs, and the clinical phenotypes differ depending on the genetic background in humans and in mice
Summary
Autoimmunity is caused by failure of immunological tolerance for self-tissue antigen. Self-reactive immune cells are normally deleted due to so-called self-tolerance system. The self-tolerance develops mainly in central and in peripheral lymphoid tissues. A negative selection to remove auto-reactive T cells is mainly accomplished in thymic medulla [1,2]. In thymic medullary epithelial cells (mTECs), expression of a number of ectopic genes encoding tissue-specific peripheral antigens (TSAs) has been observed. When the self-tolerance breaks down due to some causes, an immune response to the self-antigen is induced, resulting in the development of autoimmune diseases
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