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1.
The Journal of the Korean Society for Transplantation ; : 234-240, 2006.
Article in Korean | WPRIM | ID: wpr-97777

ABSTRACT

Purpose: The aim of the present study was to identify whether the percentages of T cell subset, the serum interferon-gamma (IFN gamma ) as a Th1 cytokine, soluble CD30 (sCD30) as a marker for activation of Th2 cytokine producing T cells, and intracellular cytokines (IL-2, IL-4) can predict the acute cellular rejection episodes of liver transplant patients. Methods: Pretransplant and posttransplant sera on days 1, 3 and 7 after surgery of 88 adult living donor liver transplant recipients were tested for the percentage of T cell subset (CD3+, CD4+ and CD8+ T cells), IL-2, IL-4 production by peripheral mononucleated cells with fluorescence activated cell sorter analysis and for the serum IFN gamma , sCD30 concentrations with commercial ELISA kits. Recipients were subdivided into three groups as control (n=51), ELE (the group which showed elevated liver enzyme but RAI score or =3. n=13). The differences in the level of cytokines among each group were analyzed. Results: The percentages of CD3+ T cell subset at preoperatively and day 1, 7 after surgery in AR were higher than those of control (P <0.05). The IL-2 production in AR was the highest and the IL-4 production was the lowest on posttransplant 7th day among three groups without significance. AR had a significantly higher pretranspant IFN gamma concentration than control (P <0.05). The pretransplant serum level of sCD30 was not different between the control and AR. However, in comparison with control, which showed a steadily decreasing serum sCD30 level after transplantation, 12 of the 14 patients in the AR showed an increase in their sCD30 levels from day 1 to day 3 after transplantation (P <.05). Conclusion: The measurement of serum IFN gamma and sCD30 during pre- and early post-LDLT period might be helpful to evaluate the risk of the occurrence of liver allograft rejection.


Subject(s)
Adult , Humans , Allografts , Cytokines , Enzyme-Linked Immunosorbent Assay , Fluorescence , Interferon-gamma , Interleukin-2 , Interleukin-4 , Liver , Living Donors , T-Lymphocytes , Transplantation
2.
Pediatric Allergy and Respiratory Disease ; : 319-326, 2001.
Article in Korean | WPRIM | ID: wpr-208399

ABSTRACT

PURPOSE: The pathogenesis of atopic dermatitis is not clearly defined yet, but the pathogenetic role of Th2 cells has been supposed. CD30 is a membrane-bound glycoprotein that may be expressed on activated T cells with a sustained expression in Th2 cells and can be released as a soluble form(sCD30). This study was done to document the changes of serum sCD30 and it's clinical significance in atopic dermatitis. METHODS: We analyzed serum sCD30, serum soluble IL-2 receptor (sIL-2R), total serum IgE and total eosinophil counts from 18 children with atopic dermatitis(AD), 15 atopic asthmatics without AD (AA), 15 atopic asthmatics with AD(AD+AA), and 14 healthy non atopics(control). We investigated the correlation of serum sCD30 levels with disease severity assessed by clinical scoring(SCORAD index) in the group of AD and AD+AA. RESULTS: The serum levels of sCD30 were significantly higher in the group of AD and AD+AA than the group of AA and control. There were no differences in serum sCD30 levels between the group of AA and control and between the group of AD and AD+AA. The serum sIL-2R levels showed no significant differences among the four groups. There was significant positive correlation between serum sCD30 and serum sIL-2R levels(P<0.05). Both serum sCD30 and serum sIL-2R levels showed no correlation with total serum IgE, total eosinophil counts, and disease severity, respectively. CONCLUSION: Serum sCD30 is elevated only in atopic dermatitis irrespective of presence of asthma. The results suggest that Th2 immune responses may involved the pathogenesis of atopic dermatitis and sCD30 may be the possible marker of atopic dermatitis.


Subject(s)
Child , Humans , Asthma , Dermatitis, Atopic , Eosinophils , Glycoproteins , Immunoglobulin E , Receptors, Interleukin-2 , T-Lymphocytes , Th2 Cells
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