Literature DB >> 12829915

High expression of TIAF-1 in chronic kidney and liver allograft rejection and in activated T-helper cells.

Judith van der Leij1, Anke van den Berg, Ester W J A Albrecht, Tjasso Blokzijl, Ramon Roozendaal, Annette S H Gouw, Koert P de Jong, Coen A Stegeman, Harry van Goor, Nan-Shan Chang, Sibrand Poppema.   

Abstract

BACKGROUND: T helper cells are important modulators of the allograft immune response. A small number of genes are already known to be differentially expressed in T helper 1 (Th1) and T helper 2 (Th2) cells, but it is likely that many other genes are functionally important. To study gene expression in Th1 and Th2 cells, we used serial analysis of gene expression. One of the differentially expressed genes was TIAF-1, which is a TGF-beta 1-induced antiapoptotic factor, known to inhibit the cytotoxic effects of tumor necrosis factor-alpha on mouse fibroblasts. We hypothesized that TIAF-1 plays a protective role against apoptosis during allograft rejection.
METHODS: We examined TIAF-1 mRNA and protein expression in kidney and liver allograft biopsy specimens from patients with chronic or acute rejection by reverse transcriptase-polymerase chain reaction and immunohistochemistry.
RESULTS: TIAF-1 mRNA and protein were not detectable in normal kidney and liver; however, the expression of TIAF-1 was up-regulated in most biopsy specimens with chronic and a few with acute allograft rejection. Immunohistochemistry for TIAF-1 revealed expression in the inflammatory infiltrate and in tubular epithelial cells.
CONCLUSIONS: TIAF-1 mRNA and protein are predominantly up-regulated in kidney and liver allografts with chronic rejection. This does not seem to be related to the cyclosporine A therapy. Expression of TIAF-1 in the lymphocytes during chronic allograft rejection may be related to the predominance of a Th2 response in this condition. The expression in the transplanted tissue may protect these cells from apoptosis.

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Year:  2003        PMID: 12829915     DOI: 10.1097/01.TP.0000069829.71088.88

Source DB:  PubMed          Journal:  Transplantation        ISSN: 0041-1337            Impact factor:   4.939


  6 in total

1.  Hypervariable genes--experimental error or hidden dynamics.

Authors:  Igor Dozmorov; Nicholas Knowlton; Yuhong Tang; Alan Shields; Parima Pathipvanich; James N Jarvis; Michael Centola
Journal:  Nucleic Acids Res       Date:  2004-10-28       Impact factor: 16.971

2.  TGF-β induces TIAF1 self-aggregation via type II receptor-independent signaling that leads to generation of amyloid β plaques in Alzheimer's disease.

Authors:  M-H Lee; S-R Lin; J-Y Chang; L Schultz; J Heath; L-J Hsu; Y-M Kuo; Q Hong; M-F Chiang; C-X Gong; C-I Sze; N-S Chang
Journal:  Cell Death Dis       Date:  2010-12-23       Impact factor: 8.469

3.  TIAF1 self-aggregation in peritumor capsule formation, spontaneous activation of SMAD-responsive promoter in p53-deficient environment, and cell death.

Authors:  J-Y Chang; M-F Chiang; S-R Lin; M-H Lee; H He; P-Y Chou; S-J Chen; Y-A Chen; L-Y Yang; F-J Lai; C-C Hsieh; T-H Hsieh; H-M Sheu; C-I Sze; N-S Chang
Journal:  Cell Death Dis       Date:  2012-04-26       Impact factor: 8.469

4.  Signatures of human regulatory T cells: an encounter with old friends and new players.

Authors:  Susanne Pfoertner; Andreas Jeron; Michael Probst-Kepper; Carlos A Guzman; Wiebke Hansen; Astrid M Westendorf; Tanja Toepfer; Andres J Schrader; Anke Franzke; Jan Buer; Robert Geffers
Journal:  Genome Biol       Date:  2006       Impact factor: 13.583

Review 5.  WWOX Phosphorylation, Signaling, and Role in Neurodegeneration.

Authors:  Chan-Chuan Liu; Pei-Chuan Ho; I-Ting Lee; Yu-An Chen; Chun-Hsien Chu; Chih-Chuan Teng; Sheng-Nan Wu; Chun-I Sze; Ming-Fu Chiang; Nan-Shan Chang
Journal:  Front Neurosci       Date:  2018-08-15       Impact factor: 4.677

6.  Self-aggregating TIAF1 in lung cancer progression.

Authors:  Qunying Hong; Li-Jin Hsu; Pei-Yi Chou; Ying-Tsen Chou; Chen-Yu Lu; Yu-An Chen; Nan-Shan Chang
Journal:  Transl Respir Med       Date:  2013-02-28
  6 in total

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