Defective T suppressor-inducer cell function in human immune deficiency virus-seropositive hemophilia patients

In human immune deficiency virus (HIV)-seropositive hemophilia patients, a low number of CD4 + lymphocytes is found, as well as a low CD4+/CD8+ ratio. In previous studies, it has been shown that antigen- specific T-helper cell (CD4+) function was present and no excessive antigen-specific T-suppressor cell (CD8+) function could be demonstrated. In this report, we studied another activity of CD4+ cells, namely the capacity to induce T-suppressor cell activity. The results clearly show a selective dysfunction of CD4+ suppressor-inducer (Tsi) cell function. Since these HIV-seropositive hemophilia patients showed the presence of activated B cells in the peripheral circulation refractory to antigen-specific T-helper cell signals and secreting specific antibodies spontaneously, we raised the hypothesis that the activated B cells in the patients activate the Tsi cells in vivo. This constant activation leads to a functional exhaustion of the Tsi cell pool.

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Defective T suppressor-inducer cell function in human immune deficiency virus-seropositive hemophilia patients

Blood ◽

10.1182/blood.v72.5.1474.1474 ◽

1988 ◽

Vol 72 (5) ◽

pp. 1474-1477 ◽

Cited By ~ 4

Author(s):

LJ Sjamsoedin-Visser ◽

CJ Heijnen ◽

BJ Zegers ◽

JW Stoop

Keyword(s):

Immune Deficiency ◽

B Cells ◽

Cell Function ◽

Suppressor Cell ◽

T Helper Cell ◽

Helper Cell ◽

Human Immune Deficiency Virus ◽

T Helper ◽

Human Immune ◽

Hiv Seropositive

Abstract In human immune deficiency virus (HIV)-seropositive hemophilia patients, a low number of CD4 + lymphocytes is found, as well as a low CD4+/CD8+ ratio. In previous studies, it has been shown that antigen- specific T-helper cell (CD4+) function was present and no excessive antigen-specific T-suppressor cell (CD8+) function could be demonstrated. In this report, we studied another activity of CD4+ cells, namely the capacity to induce T-suppressor cell activity. The results clearly show a selective dysfunction of CD4+ suppressor-inducer (Tsi) cell function. Since these HIV-seropositive hemophilia patients showed the presence of activated B cells in the peripheral circulation refractory to antigen-specific T-helper cell signals and secreting specific antibodies spontaneously, we raised the hypothesis that the activated B cells in the patients activate the Tsi cells in vivo. This constant activation leads to a functional exhaustion of the Tsi cell pool.

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Defect in B cell function in HTLV III/LAV positive hemophilia patients

Blood ◽

10.1182/blood.v69.5.1388.1388 ◽

1987 ◽

Vol 69 (5) ◽

pp. 1388-1393 ◽

Cited By ~ 9

Author(s):

EJ Sjamsoedin-Visser ◽

CJ Heijnen ◽

BJ Zegers ◽

JW Stoop

Keyword(s):

B Cells ◽

Peripheral Blood ◽

Cell Function ◽

Cell Activity ◽

Peripheral Blood Lymphocytes ◽

T Helper Cell ◽

Helper Cell ◽

T Helper

Abstract The capacity of the peripheral blood lymphocytes (PBL) to generate an antibody response in vitro T cell-dependent antigen ovalbumin was studied in 12 severe hemophilia patients who were otherwise in good health. PBL from four of 12 patients were not capable of generating such a response after stimulation in vitro, whereas all controls were normal. This negative plaque-forming cell (PFC) response coincided with the presence of antibodies directed toward human T-lymphotropic virus III/lymphadenopathy-associated virus (HTLV-III/LAV). Only one patient with antibodies against HTLV-III/LAV had a normal PFC response. The negative PFC response was not due to a deficient T helper cell activity, nor to an excessive T suppressor cell function. However, in the peripheral blood of these four patients, the presence of activated B cells that are refractory to antigen-specific T helper cell signals and secrete specific antibodies spontaneously could be demonstrated. Most of the patients showed a hyperimmunoglobulinemia. No correlation between the T4/T8 ratio and the level of the PFC response was demonstrable. From the data obtained in these investigations we raise the hypothesis that infection with HTLV-III/LAV in hemophilia patients will lead to in vivo (pre)activation of B cells that results in unresponsiveness or decreased response to antigen-specific signals.

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Evaluation of B-cell, T-helper-cell, and T-suppressor-cell function in patients with Graves' disease before and after treatment with anti-thyroid drugs

Clinical Immunology and Immunopathology ◽

10.1016/0090-1229(82)90186-6 ◽

1982 ◽

Vol 25 (2) ◽

pp. 232-242 ◽

Cited By ~ 7

Author(s):

B.M. Jones ◽

C.S. Teng ◽

R.T.T. Yeung

Keyword(s):

B Cell ◽

Cell Function ◽

Suppressor Cell ◽

T Helper Cell ◽

Helper Cell ◽

Graves Disease ◽

T Helper ◽

Before And After

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Defect in B cell function in HTLV III/LAV positive hemophilia patients

Blood ◽

10.1182/blood.v69.5.1388.bloodjournal6951388 ◽

1987 ◽

Vol 69 (5) ◽

pp. 1388-1393

Author(s):

EJ Sjamsoedin-Visser ◽

CJ Heijnen ◽

BJ Zegers ◽

JW Stoop

Keyword(s):

B Cells ◽

Peripheral Blood ◽

Cell Function ◽

Cell Activity ◽

Peripheral Blood Lymphocytes ◽

T Helper Cell ◽

Helper Cell ◽

T Helper

The capacity of the peripheral blood lymphocytes (PBL) to generate an antibody response in vitro T cell-dependent antigen ovalbumin was studied in 12 severe hemophilia patients who were otherwise in good health. PBL from four of 12 patients were not capable of generating such a response after stimulation in vitro, whereas all controls were normal. This negative plaque-forming cell (PFC) response coincided with the presence of antibodies directed toward human T-lymphotropic virus III/lymphadenopathy-associated virus (HTLV-III/LAV). Only one patient with antibodies against HTLV-III/LAV had a normal PFC response. The negative PFC response was not due to a deficient T helper cell activity, nor to an excessive T suppressor cell function. However, in the peripheral blood of these four patients, the presence of activated B cells that are refractory to antigen-specific T helper cell signals and secrete specific antibodies spontaneously could be demonstrated. Most of the patients showed a hyperimmunoglobulinemia. No correlation between the T4/T8 ratio and the level of the PFC response was demonstrable. From the data obtained in these investigations we raise the hypothesis that infection with HTLV-III/LAV in hemophilia patients will lead to in vivo (pre)activation of B cells that results in unresponsiveness or decreased response to antigen-specific signals.

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