Imbalance of T-cell subpopulations and defective pokeweed mitogen-induced B-cell differentiation after bone marrow transplantation in man

Andrea Bacigalupo, Maria C. Mingari, Lorenzo Moretta, Marina Podesta', Maria T. Van Lint, Giovanna Piaggio, Maria R. Raffo, Alberto Marmont

Research output: Contribution to journalArticlepeer-review

Abstract

Peripheral blood T-cell subpopulations were studied in eight patients undergoing bone marrow transplantation (BMT) for severe aplastic anemia (SAA) or acute leukemia (AL). Seven received an allogeneic graft and one a syngeneic graft: seven showed clinical and pathological signs of graft versus host disease (GvHD) and a marked imbalance in T-cell subpopulations. In spite of normal numbers of circulating unfractionated T cells, T lymphocytes with receptors for IgG (TG cells) were increased 2- to 5-fold, whereas T cells with receptors for IgM (TM cells) showed a 2- to 20-fold decrease. The TM-TG imbalance paralleled the development of GvHD. The patient who received the syngeneic graft showed no TM-TG imbalance and no signs of GvHD. In addition pokeweed mitogen (PWM)-induced B-cell differentiation in vitro was severely impaired in these patients in the presence of either autologous or normal allogeneic T cells. Patients' T cells did not provide adequate help for autologous or normal B cells either in the presence or absence of TG cells. The patients' purified TG cells were capable of suppressing normal B-cell responses to PWM but to a lesser degree than normal TG cells. The imbalance of T-cell subpopulations with defective helper activity and the impaired B-cell function may play an important role in the development of immunodeficiency after bone marrow transplantation and particularly during GvHD.

Original languageEnglish
Pages (from-to)137-145
Number of pages9
JournalClinical Immunology and Immunopathology
Volume20
Issue number2
DOIs
Publication statusPublished - 1981

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Pathology and Forensic Medicine

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