PMID- 11326474
OWN - NLM
STAT- MEDLINE
DCOM- 20010906
LR  - 20170112
IS  - 0392-856X (Print)
IS  - 0392-856X (Linking)
VI  - 19
IP  - 2
DP  - 2001 Mar-Apr
TI  - Tumor necrosis factor-alpha and receptors for it in labial salivary glands in 
      Sjogren's syndrome.
PG  - 131-7
AB  - OBJECTIVE: Modulation of TNF-alpha by neutralizing antibodies, soluble receptors 
      and TNFR: Fc fusion proteins are being developed for the therapeutic modulation 
      of immune inflammation. It is becoming increasingly important to understand the 
      state and involvement of the TNF-alpha/TNFR system in various rheumatic diseases. 
      Tumor necrosis factor-alpha (TNF-alpha) affects its target cells through binding 
      to two different receptors, TNFR-p55 and TNFR-p75. Mitogenic, cytostatic and 
      cytotoxic effects of TNF-alpha on various cells have been reported. In Sjogren's 
      syndrome (SS) focal sialadenitis leads to salivary gland destruction and loss of 
      function. Although TNF-alpha is one possible mediator in these processes, nothing 
      is known about the spatial distribution of TNF-alpha in relation to its 
      receptors/target cells in salivary gland tissue. METHODS: Labial salivary glands 
      (LSG) were obtained from 16 SS patients and 13 healthy controls and stained using 
      the immunohistochemical peroxidase-anti-peroxidase (PAP) method for TNF-alpha, 
      TNFR-p55 and TNFR-p75. RESULTS: TNF-alpha, TNFR-p55 and TNFR-p75 staining was 
      absent, weak or relatively inextensive in controls compared to SS patients. 
      Infiltrating mononuclear inflammatory cells in SS patients displayed moderate to 
      strong TNF-alpha and TNFR expression. In addition, resident vascular endothelial 
      cells, ductal epithelial cells and fibroblasts co-expressed TNF-alpha and TNFR. 
      In contrast, acinar end piece cells did not express TNF-alpha or TNFR-p75 
      although TNFR-p55 was expressed. CONCLUSION: The interrelated localization of TNF 
      receptors and their ligand TNF-alpha in inflammatory and in endothelial cells 
      suggests a proinflammatory role of TNF-alpha in SS. The expression of TNF-alpha 
      and its receptors in fibroblasts and ductal cells may contribute to ductal 
      hyperplasia and glandular fibrosis. However, in contrast to expectations, the 
      cellular localization of the TNF-alpha/TNRF system argues against its role in 
      acinar cell atrophy.
FAU - Koski, H
AU  - Koski H
AD  - Institute of Biomedicine, Department of Anatomy, University of Helsinki, Finland. 
      hannele.koski@helsinki.fi
FAU - Janin, A
AU  - Janin A
FAU - Humphreys-Beher, M G
AU  - Humphreys-Beher MG
FAU - Sorsa, T
AU  - Sorsa T
FAU - Malmstrom, M
AU  - Malmstrom M
FAU - Konttinen, Y T
AU  - Konttinen YT
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Italy
TA  - Clin Exp Rheumatol
JT  - Clinical and experimental rheumatology
JID - 8308521
RN  - 0 (Antigens, CD)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Antigens, CD/*analysis/immunology
MH  - Apoptosis/immunology
MH  - Atrophy
MH  - Biopsy
MH  - Humans
MH  - Immunoenzyme Techniques
MH  - Receptors, Tumor Necrosis Factor/*analysis/immunology
MH  - Receptors, Tumor Necrosis Factor, Type II
MH  - Salivary Glands/*chemistry/immunology/pathology
MH  - Sjogren's Syndrome/*immunology/pathology
MH  - Tumor Necrosis Factor-alpha/*analysis/immunology
EDAT- 2001/05/01 10:00
MHDA- 2001/09/08 10:01
CRDT- 2001/05/01 10:00
PHST- 2001/05/01 10:00 [pubmed]
PHST- 2001/09/08 10:01 [medline]
PHST- 2001/05/01 10:00 [entrez]
PST - ppublish
SO  - Clin Exp Rheumatol. 2001 Mar-Apr;19(2):131-7.