CGRP-Mediated Prolactin Upregulation: a Possible Pathomechanism in IgG4-Related Disease
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ORIGINAL ARTICLE
CGRP-Mediated Prolactin Upregulation: a Possible Pathomechanism in IgG4-Related Disease Qicai Liu ,1 Yunfeng Lin,2 Sheng Zhang,3,4,9 Min Chen,5 Qingquan Chen,5 Hongbin Rui,6 Fang Wang,7 Xiaoting Lv,8 and Feng Gao3,4,9
(Received August 21, 2020; accepted September 24, 2020)
Abstract—Similar to other immune-mediated diseases, IgG4-related disease (IgG4-RD) is the disease that develops in genetically susceptible individuals exposed to external or endogenous antigens. In the present study, it was confirmed that MAG (myelinassociated glycoprotein) antibodies (IgG, IgG4, and IgM) were detected by immunofluorescence (IFA) in serum of the patients with IgG4-RD. In vivo, the levels of prolactin and Th2 cytokines in CGRP+/− rats were higher than those in wild-type. Our findings indicate that the presence of CGRP-deficiency-mediated MAG antibodies is a probable molecular basis for the initial events which were triggered in IgG4-RD immune responses via prolactin upregulation. KEY WORDS: MAG antibody; CGRP; prolactin; IgG4-RD.
INTRODUCTION Co-First: Qicai Liu and Yunfeng Lin 1
Center for Reproductive Medicine, 1st Affiliated Hospital, Fujian Medical University, Fuzhou, China 2 Department of Neonatology, Fujian Provincial Maternity and Children’s Hospital, Affiliated Hospital of Fujian Medical University, Fuzhou, China 3 Department of Pathology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China 4 Department of Pathology, 1st Affiliated Hospital, Fujian Medical University, 20 Chazhong Road, Fuzhou, 350005, Fujian, China 5 Department of Laboratory Medicine, Medical Technology and Engineering College, Fujian Medical University, Fuzhou, China 6 Department of Rheumatism, 1st Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China 7 Department of Pharmaceutical Analysis, Fujian Medical University, Fuzhou, China 8 Department of Respiratory and Critical Care Medicine, 1st Affiliated Hospital, Fujian Medical University, Fuzhou, China 9 To whom correspondence should be addressed at Department of Pathology, 1st Affiliated Hospital, Fujian Medical University, 20 Chazhong Road, Fuzhou, 350005, Fujian, China. E-mails: [email protected]; [email protected]
IgG4-related disease (IgG4-RD) is a chronic and progressive autoimmune disease involving multiple organs or tissues. The pathological hallmark of this disease is painless space-occupying peripheral neuritis and obstructive vasculitis [1, 2]. Study about its pathogenic mechanism is almost blank. Calcitonin gene-related peptide (CGRP) is a newly discovered neurotransmitter with negative regulatory function. In a prior study, we highlighted the potential importance of CGRP mutations and lower expression involved in inducing obliterative vasculitis and perineural inflammation [3]. Here, we report our anatomical and functional observations suggesting a mechanism by which this nerve injury-evoked “phenotypic switching” induces contrasting neuropathic painless phenotypes in IgG4-RD [4, 5]. As known, CGRP are crucial components in the pat
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