DEFICIENT T-CELL GRANULOCYTE-MACROPHAGE COLONY STIMULATING FACTOR PRODUCTION IN ALLOGENEIC BONE-MARROW TRANSPLANT RECIPIENTS

被引:13
|
作者
THOMAS, S
CLARK, SC
RAPPEPORT, JM
NATHAN, DG
EMERSON, SG
机构
[1] UNIV MICHIGAN, MED CTR,DIV HEMATOL ONCOL,1150 W MED CTR DR, 5510B MSRB, ANN ARBOR, MI 48109 USA
[2] BRIGHAM & WOMENS HOSP, DIV HEMATOL, BOSTON, MA 02115 USA
[3] UNIV MICHIGAN, MED CTR, DEPT INTERNAL MED & PEDIAT, DIV HEMATOL, ANN ARBOR, MI 48109 USA
[4] GENET INST, CAMBRIDGE, MA 02140 USA
[5] UNIV MICHIGAN, MED CTR, DEPT INTERNAL MED & PEDIAT, DIV ONCOL, ANN ARBOR, MI 48109 USA
[6] HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV PEDIAT ONCOL, BOSTON, MA 02115 USA
[7] CHILDRENS HOSP MED CTR, DEPT MED, BOSTON, MA 02115 USA
关键词
D O I
10.1097/00007890-199004000-00010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The proliferation and differentiation of donor hematopoietic progenitor cells in bone marrow transplantation (BMT) recipients is influenced by hematopoietic growth factors, which could derive from either T cells or adherent stromal bone marrow cells, or both. In this study of 20 BMT recipients, we asked whether T lymphocytes arising from donor bone marrow grafts were able to express normal levels of granulocyte-macro- phage colony stimulating factor (GM-CSF) mRNA, and to secrete normal levels of soluble GM-CSF in response to the mitogen phytohemagglutinin. We have found that T cells obtained up to 18 months following BMT express little or no PHA-induced GM-CSF message. T cell GM- CSF secretion in response to PHA is also reduced or absent. This T cell GM-CSF defect was observed in all patients studied, whether or not donor bone marrows had undergone T cell depletion. This defect likely reflects a broader deficit in mitogen-induced lymphokine production. This defect likely contributes to BMT recipients’ blunted responses to infections, and contributes to graft failure in T cell-depleted transplants. © 1990 by Williams and Wilkins.
引用
收藏
页码:703 / 708
页数:6
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