Imbalances Within the Peripheral Blood T-Helper (CD4+) and T-Suppressor (CD8 + ) Cell Populations in the Reconstitution Phase After Human Bone Marrow Transplantation

• Published in: Blood Vol. 71; no. 5; pp. 1196 - 1200
• Main Authors: Velardi, Andrea, Terenzi, Adelmo, Cucciaioni, Speranza, Millo, Romano, Grossi, Carlo E., Grignani, Fausto, Martelli, Massimo F.
• Format: Journal Article
• Language: English
• Published: Washington, DC Elsevier Inc 01.05.1988; The Americain Society of Hematology
• Subjects: Adolescent; Adult; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Bone Marrow Transplantation; Bone marrow, stem cells transplantation. Graft versus host reaction; Child; Female; Humans; Interleukin-2 - biosynthesis; Leukocyte Count; Male; Medical sciences; Middle Aged; Postoperative Period; T-Lymphocytes, Helper-Inducer - pathology; T-Lymphocytes, Regulatory - pathology; Transfusions. Complications. Transfusion reactions. Cell and gene therapy; Human; T-Lymphocyte; Homograft; Bone marrow; Various treatments; Helper cell; Suppressive cell; Hemopathy; Cell subpopulation
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood.V71.5.1196.1196

Peripheral blood T cell subsets were evaluated in 11 patients during the reconstitution phase after allogeneic bone marrow transplantation and compared with 11 age-matched controls. The proportion of cells coexpressing Leu7 and CD11b (C3bi receptor) markers was determined within the CD4+ (T-helper) and the CD8+ (T-suppressor) subsets by two-color immunofluorescence analysis. CD4+ and CD8+ T cells reached normal or near-normal values within the first year posttransplant. In contrast to normal controls, however, most of the cells in both subsets coexpressed the Leu7 and CD11b markers. T cells with such phenotype display the morphological features of granular lymphocytes (GLs) and a functional inability to produce interleukin 2 (IL 2). These T cell imbalances were not related to graft v host disease (GvHD) or to clinically detectable virus infections and may account for some defects of cellular and humoral immunity that occur after bone marrow transplantation.