Defective control of Epstein-Barr virus-infected B cell growth in patients with X-linked lymphoproliferative disease

N. Yasuda, P. K. Lai, J. Rogers, D. T. Purtlo

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

We studied the cellular function and lymphokine production of T cells from patients with X-linked lymphoproliferative disease (XLP) when activated by the challenge with Epstein-Barr virus (EBV) infection. We used an assay system in which T cells were stimulated with membrane antigens of autologous EBV-infected B lymphoblastoid cell lines (B-LCL) and we examined cellular and humoral factors derived from the stimulated T cells which control the growth of EBV-infected B-LCL. Immunoglobulin secretion from the autologous B-LCL was suppressed with radiosensitive suppressor cells in the patients with XLP. The degree of suppression was correlated with the immunoglobulin levels in the serum of the patients with acquired hypogammaglobulinaemia (P < 0.05). In addition, T cells from the patients with XLP failed to produce interferon-gamma (IFN-γ) (P < 0.001). Moreover, the T cell supernatants from the patients with XLP were less potent to inhibit the B-LCL growth. This diminished inhibition of the B-LCL growth was correlated well with the decreased concentration of IFN-γ in the T cell supernatants. These findings suggest that suppressor cells may be activated in the patients with the hypogammaglobulinemia phenotype of XLP, but the frequent development of B cell lymphoma in hypogammaglobulinaemia indicate that immunoglobulin suppression may not exert enough pressure on the in vivo growth of EBV-infected B cells. The defective secretion of IFN-γ may be, at least partially, responsible for the abnormal cytotoxic T cell and natural killer activities found in the patients with XLP, and may indicate the clinical evaluation about the preventive injection of IFN-γ against the development of malignant lymphoma.

Original languageEnglish (US)
Pages (from-to)10-16
Number of pages7
JournalClinical and Experimental Immunology
Volume83
Issue number1
StatePublished - Jan 1 1991

Fingerprint

Lymphoproliferative Disorders
Human Herpesvirus 4
B-Lymphocytes
T-Lymphocytes
Interferon-gamma
Growth
Cell Line
Immunoglobulins
Agammaglobulinemia
Common Variable Immunodeficiency
Natural Killer T-Cells
Epstein-Barr Virus Infections
Lymphokines
B-Cell Lymphoma
Lymphoma
Phenotype
Pressure
Injections
Serum

Keywords

  • Epstein-Barr virus
  • Interferon-gamma
  • Suppressor T cells
  • X-linked lymphoproliferative disease

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Defective control of Epstein-Barr virus-infected B cell growth in patients with X-linked lymphoproliferative disease. / Yasuda, N.; Lai, P. K.; Rogers, J.; Purtlo, D. T.

In: Clinical and Experimental Immunology, Vol. 83, No. 1, 01.01.1991, p. 10-16.

Research output: Contribution to journalArticle

@article{989450198ce74b74bf69126c364e75cd,
title = "Defective control of Epstein-Barr virus-infected B cell growth in patients with X-linked lymphoproliferative disease",
abstract = "We studied the cellular function and lymphokine production of T cells from patients with X-linked lymphoproliferative disease (XLP) when activated by the challenge with Epstein-Barr virus (EBV) infection. We used an assay system in which T cells were stimulated with membrane antigens of autologous EBV-infected B lymphoblastoid cell lines (B-LCL) and we examined cellular and humoral factors derived from the stimulated T cells which control the growth of EBV-infected B-LCL. Immunoglobulin secretion from the autologous B-LCL was suppressed with radiosensitive suppressor cells in the patients with XLP. The degree of suppression was correlated with the immunoglobulin levels in the serum of the patients with acquired hypogammaglobulinaemia (P < 0.05). In addition, T cells from the patients with XLP failed to produce interferon-gamma (IFN-γ) (P < 0.001). Moreover, the T cell supernatants from the patients with XLP were less potent to inhibit the B-LCL growth. This diminished inhibition of the B-LCL growth was correlated well with the decreased concentration of IFN-γ in the T cell supernatants. These findings suggest that suppressor cells may be activated in the patients with the hypogammaglobulinemia phenotype of XLP, but the frequent development of B cell lymphoma in hypogammaglobulinaemia indicate that immunoglobulin suppression may not exert enough pressure on the in vivo growth of EBV-infected B cells. The defective secretion of IFN-γ may be, at least partially, responsible for the abnormal cytotoxic T cell and natural killer activities found in the patients with XLP, and may indicate the clinical evaluation about the preventive injection of IFN-γ against the development of malignant lymphoma.",
keywords = "Epstein-Barr virus, Interferon-gamma, Suppressor T cells, X-linked lymphoproliferative disease",
author = "N. Yasuda and Lai, {P. K.} and J. Rogers and Purtlo, {D. T.}",
year = "1991",
month = "1",
day = "1",
language = "English (US)",
volume = "83",
pages = "10--16",
journal = "Clinical and Experimental Immunology",
issn = "0009-9104",
publisher = "Wiley-Blackwell",
number = "1",

}

TY - JOUR

T1 - Defective control of Epstein-Barr virus-infected B cell growth in patients with X-linked lymphoproliferative disease

AU - Yasuda, N.

AU - Lai, P. K.

AU - Rogers, J.

AU - Purtlo, D. T.

PY - 1991/1/1

Y1 - 1991/1/1

N2 - We studied the cellular function and lymphokine production of T cells from patients with X-linked lymphoproliferative disease (XLP) when activated by the challenge with Epstein-Barr virus (EBV) infection. We used an assay system in which T cells were stimulated with membrane antigens of autologous EBV-infected B lymphoblastoid cell lines (B-LCL) and we examined cellular and humoral factors derived from the stimulated T cells which control the growth of EBV-infected B-LCL. Immunoglobulin secretion from the autologous B-LCL was suppressed with radiosensitive suppressor cells in the patients with XLP. The degree of suppression was correlated with the immunoglobulin levels in the serum of the patients with acquired hypogammaglobulinaemia (P < 0.05). In addition, T cells from the patients with XLP failed to produce interferon-gamma (IFN-γ) (P < 0.001). Moreover, the T cell supernatants from the patients with XLP were less potent to inhibit the B-LCL growth. This diminished inhibition of the B-LCL growth was correlated well with the decreased concentration of IFN-γ in the T cell supernatants. These findings suggest that suppressor cells may be activated in the patients with the hypogammaglobulinemia phenotype of XLP, but the frequent development of B cell lymphoma in hypogammaglobulinaemia indicate that immunoglobulin suppression may not exert enough pressure on the in vivo growth of EBV-infected B cells. The defective secretion of IFN-γ may be, at least partially, responsible for the abnormal cytotoxic T cell and natural killer activities found in the patients with XLP, and may indicate the clinical evaluation about the preventive injection of IFN-γ against the development of malignant lymphoma.

AB - We studied the cellular function and lymphokine production of T cells from patients with X-linked lymphoproliferative disease (XLP) when activated by the challenge with Epstein-Barr virus (EBV) infection. We used an assay system in which T cells were stimulated with membrane antigens of autologous EBV-infected B lymphoblastoid cell lines (B-LCL) and we examined cellular and humoral factors derived from the stimulated T cells which control the growth of EBV-infected B-LCL. Immunoglobulin secretion from the autologous B-LCL was suppressed with radiosensitive suppressor cells in the patients with XLP. The degree of suppression was correlated with the immunoglobulin levels in the serum of the patients with acquired hypogammaglobulinaemia (P < 0.05). In addition, T cells from the patients with XLP failed to produce interferon-gamma (IFN-γ) (P < 0.001). Moreover, the T cell supernatants from the patients with XLP were less potent to inhibit the B-LCL growth. This diminished inhibition of the B-LCL growth was correlated well with the decreased concentration of IFN-γ in the T cell supernatants. These findings suggest that suppressor cells may be activated in the patients with the hypogammaglobulinemia phenotype of XLP, but the frequent development of B cell lymphoma in hypogammaglobulinaemia indicate that immunoglobulin suppression may not exert enough pressure on the in vivo growth of EBV-infected B cells. The defective secretion of IFN-γ may be, at least partially, responsible for the abnormal cytotoxic T cell and natural killer activities found in the patients with XLP, and may indicate the clinical evaluation about the preventive injection of IFN-γ against the development of malignant lymphoma.

KW - Epstein-Barr virus

KW - Interferon-gamma

KW - Suppressor T cells

KW - X-linked lymphoproliferative disease

UR - http://www.scopus.com/inward/record.url?scp=0025977615&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025977615&partnerID=8YFLogxK

M3 - Article

C2 - 1846327

AN - SCOPUS:0025977615

VL - 83

SP - 10

EP - 16

JO - Clinical and Experimental Immunology

JF - Clinical and Experimental Immunology

SN - 0009-9104

IS - 1

ER -