Phenotype and serine esterase production of human cardiac allograft-infiltrating lymphocytes.
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.(ABSTRACT TRUNCATED AT 250 WORDS)
Carlquist
J F
JF
Department of Medicine, University of Utah School of Medicine, Salt Lake City.
Greenwood
J H
JH
Hammond
E H
EH
Anderson
J L
JL
D015496:CD4-Positive T-Lymphocytes / Q000473:pathology; D004950:Esterases / Q000096:biosynthesis* / Q000235:genetics; D006680:HLA Antigens / Q000032:analysis; D016027:Heart Transplantation / Q000473:pathology*; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis; D007143:Immunoglobulin Heavy Chains / Q000032:analysis; D016130:Immunophenotyping; D007376:Interleukin-2; D015979:Killer Cells, Lymphokine-Activated / Q000473:pathology; D007694:Killer Cells, Natural / Q000473:pathology; D008213:Lymphocyte Activation; D009206:Myocardium / Q000473:pathology; D010641:Phenotype; D016176:T-Lymphocyte Subsets / Q000145:classification* / Q000201:enzymology* / Q000473:pathology; D013602:T-Lymphocytes, Cytotoxic / Q000473:pathology; D014184:Transplantation, Homologous
D006680:HLA Antigens; D007074:Immunoglobulin G; D007143:Immunoglobulin Heavy Chains; D007376:Interleukin-2; D004950:Esterases; C022635:serine esterase