Expression of CCL21 and 5′-Nase on pancreatic lymphatics in nonobese diabetic mice

被引:10
作者
Qu, P [1 ]
Ji, RC [1 ]
Kato, S [1 ]
机构
[1] Oita Univ, Div Morphol Anal, Dept Anat Biol & Med, Fac Med, Hasama, Oita 8795593, Japan
关键词
5 '-nucleotidase; lymphatic endothelial cell; nonobese diabetic mouse; pancreas; podoplanin; secondary lymphoid tissue chemokine;
D O I
10.1097/01.mpa.0000169728.71359.63
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Objectives: To obtain better insight into the modulation of lymphatic endothelial cells during the autoimmune process, alterations of the structures and histochemical features in the pancreatic lymphatics were studied in nonobese diabetic ( NOD) mice. Methods: The expression of secondary lymphoid tissue chemokine (SLC/CCL21) and 5'-nucleotidase (5'-Nase) on pancreatic lymphatics was examined by histochemistry and immunoblot in NOD mice. Results: As insulitis developed, the increased expression of CCL21 and podoplanin on pancreatic lymphatics was consistent with the increased number of cytoplasmic protrusions and vesicles, whereas 5'-Nase activity of lymphatics seemed to become decreased. The expression of CCL21 protein also showed an age-dependent increase in NOD pancreas, even though it was undetectable in normal controls. During the period of severe infiltration, reaction products of CCL21 and podoplanin were detected in the nucleus and cytoplasm of lymphatic endothelial cells. Dendritic cells and T lymphocytes frequently penetrated through the slender walls of lymphatics and adhered to the lymphatic luminal surfaces, precipitating with few 5'-Nase particles. In contrast to wild-type NOD mice, complete Freund adjuvant administration reduced CCL21 expression in NOD pancreas, suppressing the entry of activated dendritic cells into lymphatics. Conclusions: These findings suggest that CCL21 and 5'-Nase may be involved in the interaction between infiltrating cells and lymphatic vessels to induce the functional changes of lymphatic endothelial cells during insulitic and diabetic development.
引用
收藏
页码:148 / 155
页数:8
相关论文
共 25 条
[1]  
BreitenederGeleff S, 1997, AM J PATHOL, V151, P1141
[2]   Endothelial induction of the T-cell chemokine CCL21 in T-cell autoimmune diseases [J].
Christopherson, KW ;
Hood, AF ;
Travers, JB ;
Ramsey, H ;
Hromas, RA .
BLOOD, 2003, 101 (03) :801-806
[3]  
Dahlén E, 1998, J IMMUNOL, V160, P3585
[4]   Cutting edge: Ectopic expression of the chemokine TCA4/SLC is sufficient to trigger lymphoid neogenesis [J].
Fan, L ;
Reilly, CR ;
Luo, Y ;
Dorf, ME ;
Lo, D .
JOURNAL OF IMMUNOLOGY, 2000, 164 (08) :3955-3959
[5]   Increase in podoplanin-expressing intestinal lymphatic vessels in inflammatory bowel disease [J].
Geleff, S ;
Schoppmann, SF ;
Oberhuber, G .
VIRCHOWS ARCHIV, 2003, 442 (03) :231-237
[6]   Hepatic expression of secondary lymphoid chemokine (CCL21) promotes the development of portal-associated lymphoid tissue in chronic inflammatory liver disease [J].
Grant, AJ ;
Goddard, S ;
Ahmed-Choudhury, J ;
Reynolds, G ;
Jackson, DG ;
Briskin, M ;
Wu, LJ ;
Hübscher, SG ;
Adams, DH .
AMERICAN JOURNAL OF PATHOLOGY, 2002, 160 (04) :1445-1455
[7]  
Hub E, 1998, AM J PATHOL, V152, P749
[8]  
Ji RC, 2005, HISTOL HISTOPATHOL, V20, P155, DOI 10.14670/HH-20.155
[9]   Application of a new 5′-Nase monoclonal antibody specific for lymphatic endothelial cells [J].
Ji, RC ;
Qu, P ;
Kato, S .
LABORATORY INVESTIGATION, 2003, 83 (11) :1681-1683
[10]   Lymphatic network and lymphangiogenesis in the gastric wall [J].
Ji, RC ;
Kato, S .
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 2003, 51 (03) :331-338