Phenotype and serine esterase production of human cardiac allograft-infiltrating lymphocytes

• Published in: The Journal of heart and lung transplantation Vol. 12; no. 5; p. 748
• Main Authors: Carlquist, J F, Greenwood, J H, Hammond, E H, Anderson, J L
• Format: Journal Article
• Language: English
• Published: United States 01.09.1993
• Subjects: CD4-Positive T-Lymphocytes - pathology; Esterases - biosynthesis; Esterases - genetics; Heart Transplantation - pathology; HLA Antigens - analysis; Humans; Immunoglobulin G - analysis; Immunoglobulin Heavy Chains - analysis; Immunophenotyping; Interleukin-2; Killer Cells, Lymphokine-Activated - pathology; Killer Cells, Natural - pathology; Lymphocyte Activation; Myocardium - pathology; Phenotype; T-Lymphocyte Subsets - classification; T-Lymphocyte Subsets - enzymology; T-Lymphocyte Subsets - pathology; T-Lymphocytes, Cytotoxic - pathology; Transplantation, Homologous
• ISSN: 1053-2498

Human cardiac allograft-infiltrating lymphocytes were studied by in vitro expansion in interleukin-2. Of 28 graft-infiltrating lymphocyte cultures from 17 recipients, 17 were comprised predominantly of CD4+ T cells and 10 predominantly CD8+ T cells; one culture had equal numbers of CD4+ and CD8+ cells. The mean percentages (+/- SE) of T-cell subsets for all cultures were as follows: CD4+, 49% +/- 29%; CD8+, 42% +/- 31%. No correlation was observed between the culture phenotype and histologic findings, length of time from transplantation, or number (or class) of mismatched HLA antigens. N-alpha-benzyloxycarbonyl-L-lysine thiobenzyl ester serine esterase (BLT-SE) is an enzyme associated with intracellular cytotoxic T-cell granules and with target-cell destruction. Sixteen cultures were tested for BLT-SE activity and had significantly increased enzyme activity as compared to untreated peripheral blood mononuclear cells from healthy control subjects (p < 0.002), or interleukin-2-treated control cells (p < 0.05). A low percentage (0.4% +/- 0.2%) of cells in the graft-infiltrating lymphocyte cultures expressed the phenotypic marker NKH-1, suggesting that the source of BLT-SE in these cultures was not natural killer or lymphokine-activated T cells. Elevated BLT-SE was observed in five of ten cultures containing predominantly CD4+ cells and five of six cultures containing predominantly CD8+ T cells. Mixed phenotype graft-infiltrating lymphocyte cultures depleted of either CD4+ or CD8+ T cells retained BLT-SE activity. Thus both CD4+ and CD8+ graft-derived T cells can produce this enzyme although much greater variability in enzyme production was seen for CD4+ T cells.