Document Detail


Effect of tumor infiltrating lymphocytes on the expression of MHC molecules in canine transmissible venereal tumor cells.
MedLine Citation:
PMID:  12052339     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Canine transmissible venereal tumor (CTVT) can be allo-transplanted across major histocompatibility complex barriers. The expression of MHC molecules is usually low in the progression (P) stage and then greatly increases during tumor regression (R). We investigated the effects of tumor infiltrating lymphocytes (TIL) on the expression of MHC molecules of CTVT cells. Isolated, viable CTVT cells were inoculated at each of 12 sites (1 x 10(8) CTVT cells per site) on the back of six, mixed-breed dogs. Tumor masses were collected every 2-3 weeks and prepared for histopathologic, immunocytochemistry, flow cytometry and immunoblotting studies. The level of MHC expression on tumor cells from different stages of growth was measured. Initially, expression of MHC I and II molecules in P phase CTVT was low. Twelve weeks post-inoculation (PI), expression increased dramatically and it continued to increase during R phase. Tumor growth slowed after 12 weeks PI and tumors entered R phase around 17 weeks PI. We hypothesize that CTVT evades host immunosurveillance and grows progressively for 12 weeks, when it becomes vulnerable and subject to the host's anti-tumor immune responses. We further demonstrated that R phase, but not P phase, TIL were closely associated with the over-expression of MHC I and II molecules by CTVT cells. The number and proportion of TIL were higher in R phase tumors. Supernatants, from R phase co-cultures (CTVT+TIL) and TIL only, promoted MHC I and II expression on P phase CTVT cells. After culturing alone for 1 month, expression of MHC classes I and II molecules in R phase CTVT cells decreased to the level of P phase CTVT cells. However, the above-mentioned supernatants restored their expression of MHC I and II molecules. In contrast, supernatants from P phase TIL or CTVT cells increased expression slightly or had no effect. Therefore, TIL, not CTVT cells, produce the effective substance (s) to promote the expression of MHC molecules by the tumor cells. Heat treated supernatant was unable to promote the expression of MHC I and II molecules by CTVT cells. In conclusion, TIL isolated from R phase CTVT secreted a heat-sensitive, soluble substance(s) that triggered over-expression of MHC I and II after 12 weeks PI. This caused the tumor to enter R phase and helped stop CTVT growth. Our findings will facilitate the understanding and further investigation of the mechanisms that initiate host immune surveillance against tumors.
Authors:
Ya-Wen Hsiao; Kuang-Wen Liao; Shao-Wen Hung; Rea-Min Chu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Veterinary immunology and immunopathology     Volume:  87     ISSN:  0165-2427     ISO Abbreviation:  Vet. Immunol. Immunopathol.     Publication Date:  2002 Aug 
Date Detail:
Created Date:  2002-06-07     Completed Date:  2002-08-01     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8002006     Medline TA:  Vet Immunol Immunopathol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  19-27     Citation Subset:  IM    
Affiliation:
Department of Veterinary Medicine, National Taiwan University, 142 Chou-San Road, Taipei 106, Taiwan, ROC.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western / veterinary
Dog Diseases / immunology*,  metabolism
Dogs
Female
Flow Cytometry / veterinary
Gene Expression Regulation / immunology*
Histocompatibility Antigens Class I / biosynthesis,  immunology*
Histocompatibility Antigens Class II / biosynthesis,  immunology*
Immunohistochemistry / veterinary
Kinetics
Lymphocyte Culture Test, Mixed / veterinary
Lymphocytes, Tumor-Infiltrating / immunology*,  metabolism
Male
Venereal Tumors, Veterinary / immunology*,  metabolism
Chemical
Reg. No./Substance:
0/Histocompatibility Antigens Class I; 0/Histocompatibility Antigens Class II

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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