| Literature DB >> 26568263 |
Qi-cai Liu1, Feng Dong2, Jian-feng Pan3, Ze-hao Zhuang4, Feng Gao5,6, Guo-zhong Liu7, Qing-quan Chen8, Shu Chen9, Shao-huang Weng9, Li-qing Lin9, Jin-tong Chen4, Min Chen10, Cheng-dan Wang11, Xin-hua Lin12.
Abstract
Type 1 autoimmune pancreatitis (AIP) is prototypic autoantibody-mediated diseases. Sclerosis accompanied by fiber deposition is generally regarded as the primary lesion in the development of obliterative vasculitis. However, why collagens or their antibodies play a crucial role in the pathogenesis of AIP has not been demonstrated. This study was performed to investigate if anti-collagen type IV antibodies (ACIVAbs) are the key factor of fiber deposition and recruit leukocytes, resulting in obliterative vasculitis in pancreas. Enzyme-linked immunosorbent analyses (ELISA) were used to measure the expression of Col IV and ACIVAbs in serum of patients with and without AIP. In vitro, adhesion and proliferation were determined by human lymphocytes incubated with Col IV and ACIVAbs. In vivo, C57BL0/6 mice were immunized with IgG-ACIVAbs, followed by analysis of clinical phenotype. IgG-ACIVAbs were recognized by the serum specimens from 12 of 22 patients with type 1 AIP, 3 of 9 patients with Crohn's disease, and 2 of 18 patients with pancreatic cancer, but not in healthy controls and acute pancreatitis. In patient's biopsy, ACIVAb staining increased and co-localized with subepithelial IgG4 deposits along the capillary walls and surrounding nerve fibers. In vitro, recombinant IgG-ACIVAbs increased leukocyte adhesion and proliferation. What is more, AIP could be induced in mice by immunization with IgG-ACIVAbs into adult mice.Entities:
Keywords: antibodies; autoimmune pancreatitis; collagen type IV; obliterative vasculitis
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Year: 2016 PMID: 26568263 DOI: 10.1007/s10753-015-0284-0
Source DB: PubMed Journal: Inflammation ISSN: 0360-3997 Impact factor: 4.092