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Autoimmune pancreatitis: expression and cellular source of profibrotic cytokines and their receptors.

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Autoimmune pancreatitis: expression and cellular source of profibrotic cytokines and their receptors. / Detlefsen, Sönke; Sipos, Bence; Zhao, Jingbo; Drewes, Asbjørn Mohr; Klöppel, Günter.

In: American Journal of Surgical Pathology, Vol. 32, No. 7, 2008, p. 986-95.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Detlefsen, S, Sipos, B, Zhao, J, Drewes, AM & Klöppel, G 2008, 'Autoimmune pancreatitis: expression and cellular source of profibrotic cytokines and their receptors.', American Journal of Surgical Pathology, vol. 32, no. 7, pp. 986-95. https://doi.org/10.1097/PAS.0b013e31815d2583

APA

Detlefsen, S., Sipos, B., Zhao, J., Drewes, A. M., & Klöppel, G. (2008). Autoimmune pancreatitis: expression and cellular source of profibrotic cytokines and their receptors. American Journal of Surgical Pathology, 32(7), 986-95. https://doi.org/10.1097/PAS.0b013e31815d2583

CBE

MLA

Vancouver

Author

Detlefsen, Sönke ; Sipos, Bence ; Zhao, Jingbo ; Drewes, Asbjørn Mohr ; Klöppel, Günter. / Autoimmune pancreatitis: expression and cellular source of profibrotic cytokines and their receptors. In: American Journal of Surgical Pathology. 2008 ; Vol. 32, No. 7. pp. 986-95.

Bibtex

@article{b910f090a4f911dd889c000ea68e967b,
title = "Autoimmune pancreatitis: expression and cellular source of profibrotic cytokines and their receptors.",
abstract = "Chronic pancreatitis is a fibrogenic disease. In autoimmune pancreatitis (AIP), a lymphoplasmacytic infiltration is followed by fibrosis. In vitro it has been shown that pancreatic stellate cells are transformed into proliferating myofibroblasts mainly by transforming growth factor beta (TGF-beta) and platelet-derived growth factor (PDGF). We studied the expression of these profibrotic cytokines, their receptors, and their cellular sources in AIP. Pancreatic tissues from 21 patients with AIP of different grades of severity were selected from a series of 52 AIP cases. Myofibroblasts (ie, activated pancreatic stellate cells), macrophages, lymphocytes, plasma cells, and the cytokines latency-associated peptide, a TGF-beta1 propeptide, TGF-beta receptor II (TGF-beta-RII), PDGF-B, and the alpha and beta isoforms of the PDGF receptor (PDGF-R alpha and PDGF-R beta) were identified immunohistochemically. Their expression and cellular distribution were related to the severity of AIP. In grade 1 and 2 AIP, macrophages and myofibroblasts expressing profibrotic cytokines and their receptors were found in periductal areas showing lymphoplasmacytic inflammation. In grade 3 AIP, there were numerous macrophages, myofibroblasts, and epithelial cells which were positive for latency-associated peptide, PDGF-B, TGF-beta-RII, PDGF-R alpha, and PDGF-R beta not only in periductal, but also in interlobular and intralobular areas. In grade 4 AIP, which is characterized by advanced fibrosis, cellularity and expression of cytokines and their receptors were greatly reduced. Our data indicate that in AIP the occurrence of myofibroblasts is intimately related to the presence of macrophages and lymphoplasmacytic cells. These cells and adjacent epithelial cells express profibrotic cytokines and their receptors, which are probably responsible for the initiation and maintenance of the fibrogenic process.",
keywords = "Adolescent, Adult, Aged, Autoimmune Diseases, Biological Markers, Female, Fibroblasts, Fibrosis, Humans, Immunoenzyme Techniques, Lymphocytes, Macrophages, Male, Middle Aged, Pancreatic Ducts, Pancreatitis, Chronic, Plasma Cells, Platelet-Derived Growth Factor, Protein-Serine-Threonine Kinases, Receptors, Transforming Growth Factor beta, Transforming Growth Factor beta1",
author = "S{\"o}nke Detlefsen and Bence Sipos and Jingbo Zhao and Drewes, {Asbj{\o}rn Mohr} and G{\"u}nter Kl{\"o}ppel",
year = "2008",
doi = "10.1097/PAS.0b013e31815d2583",
language = "English",
volume = "32",
pages = "986--95",
journal = "American Journal of Surgical Pathology",
issn = "0147-5185",
publisher = "LIPPINCOTT WILLIAMS & WILKINS",
number = "7",

}

RIS

TY - JOUR

T1 - Autoimmune pancreatitis: expression and cellular source of profibrotic cytokines and their receptors.

AU - Detlefsen, Sönke

AU - Sipos, Bence

AU - Zhao, Jingbo

AU - Drewes, Asbjørn Mohr

AU - Klöppel, Günter

PY - 2008

Y1 - 2008

N2 - Chronic pancreatitis is a fibrogenic disease. In autoimmune pancreatitis (AIP), a lymphoplasmacytic infiltration is followed by fibrosis. In vitro it has been shown that pancreatic stellate cells are transformed into proliferating myofibroblasts mainly by transforming growth factor beta (TGF-beta) and platelet-derived growth factor (PDGF). We studied the expression of these profibrotic cytokines, their receptors, and their cellular sources in AIP. Pancreatic tissues from 21 patients with AIP of different grades of severity were selected from a series of 52 AIP cases. Myofibroblasts (ie, activated pancreatic stellate cells), macrophages, lymphocytes, plasma cells, and the cytokines latency-associated peptide, a TGF-beta1 propeptide, TGF-beta receptor II (TGF-beta-RII), PDGF-B, and the alpha and beta isoforms of the PDGF receptor (PDGF-R alpha and PDGF-R beta) were identified immunohistochemically. Their expression and cellular distribution were related to the severity of AIP. In grade 1 and 2 AIP, macrophages and myofibroblasts expressing profibrotic cytokines and their receptors were found in periductal areas showing lymphoplasmacytic inflammation. In grade 3 AIP, there were numerous macrophages, myofibroblasts, and epithelial cells which were positive for latency-associated peptide, PDGF-B, TGF-beta-RII, PDGF-R alpha, and PDGF-R beta not only in periductal, but also in interlobular and intralobular areas. In grade 4 AIP, which is characterized by advanced fibrosis, cellularity and expression of cytokines and their receptors were greatly reduced. Our data indicate that in AIP the occurrence of myofibroblasts is intimately related to the presence of macrophages and lymphoplasmacytic cells. These cells and adjacent epithelial cells express profibrotic cytokines and their receptors, which are probably responsible for the initiation and maintenance of the fibrogenic process.

AB - Chronic pancreatitis is a fibrogenic disease. In autoimmune pancreatitis (AIP), a lymphoplasmacytic infiltration is followed by fibrosis. In vitro it has been shown that pancreatic stellate cells are transformed into proliferating myofibroblasts mainly by transforming growth factor beta (TGF-beta) and platelet-derived growth factor (PDGF). We studied the expression of these profibrotic cytokines, their receptors, and their cellular sources in AIP. Pancreatic tissues from 21 patients with AIP of different grades of severity were selected from a series of 52 AIP cases. Myofibroblasts (ie, activated pancreatic stellate cells), macrophages, lymphocytes, plasma cells, and the cytokines latency-associated peptide, a TGF-beta1 propeptide, TGF-beta receptor II (TGF-beta-RII), PDGF-B, and the alpha and beta isoforms of the PDGF receptor (PDGF-R alpha and PDGF-R beta) were identified immunohistochemically. Their expression and cellular distribution were related to the severity of AIP. In grade 1 and 2 AIP, macrophages and myofibroblasts expressing profibrotic cytokines and their receptors were found in periductal areas showing lymphoplasmacytic inflammation. In grade 3 AIP, there were numerous macrophages, myofibroblasts, and epithelial cells which were positive for latency-associated peptide, PDGF-B, TGF-beta-RII, PDGF-R alpha, and PDGF-R beta not only in periductal, but also in interlobular and intralobular areas. In grade 4 AIP, which is characterized by advanced fibrosis, cellularity and expression of cytokines and their receptors were greatly reduced. Our data indicate that in AIP the occurrence of myofibroblasts is intimately related to the presence of macrophages and lymphoplasmacytic cells. These cells and adjacent epithelial cells express profibrotic cytokines and their receptors, which are probably responsible for the initiation and maintenance of the fibrogenic process.

KW - Adolescent

KW - Adult

KW - Aged

KW - Autoimmune Diseases

KW - Biological Markers

KW - Female

KW - Fibroblasts

KW - Fibrosis

KW - Humans

KW - Immunoenzyme Techniques

KW - Lymphocytes

KW - Macrophages

KW - Male

KW - Middle Aged

KW - Pancreatic Ducts

KW - Pancreatitis, Chronic

KW - Plasma Cells

KW - Platelet-Derived Growth Factor

KW - Protein-Serine-Threonine Kinases

KW - Receptors, Transforming Growth Factor beta

KW - Transforming Growth Factor beta1

U2 - 10.1097/PAS.0b013e31815d2583

DO - 10.1097/PAS.0b013e31815d2583

M3 - Journal article

C2 - 18460977

VL - 32

SP - 986

EP - 995

JO - American Journal of Surgical Pathology

JF - American Journal of Surgical Pathology

SN - 0147-5185

IS - 7

ER -