Circulating Suppressor Cells in Aplastic Anemia

Górski, Andrzej; Rowińska, D; Skopińska, E; Orłowski, T

doi:10.1159/000460485

Cited by 2 publications

(2 citation statements)

References 5 publications

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“…The high rate of seroconversion among HCV RT-PCR positive patients suggests that humoral immunity may be normal in AA. A number of immunologic abnormalities have been observed in AA patients including decreased numbers of circulating B lymphocytes, increased numbers of activated suppressor/cytotoxic T lymphocytes in the blood, defective macrophage differentiation, and decreased circulating levels of interleukin-1 [12][13][14][15][16][17]. In addition, AA patients often receive immunosuppressive medications as part of their treatment; many of our patients were treated with glucocorticoids prior to their referral.…”

Section: Discussionmentioning

confidence: 98%

Hepatitis C virus infection in acquired aplastic anemia

et al. 1998

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Hepatitis-associated aplastic anemia (HAAA) is an uncommon disorder that usually is not due to hepatitis A or B virus infection. Hepatitis C virus (HCV) seropositivity is infrequently observed in aplastic anemia (AA) patients who have not been extensively transfused. However, HCV seropositivity may not be detected until several weeks or months after viral infection and AA patients may exhibit defective humoral immunity. Therefore, we evaluated sera from AA patients for the presence of HCV viremia using a reverse transcriptase polymerase chain reaction (RT-PCR) based assay and several serologic assays for HCV antibodies. Serum samples from 90 AA patients who presented to the UCLA Medical Center between March 1984 and February 1990 were analyzed. Overall, 17 patients were found to have HCV viremia by RT-PCR assay, of whom 14 had a positive second-generation HCV enzyme immunoassay (EIA-2) and only 6 were EIA-1 reactive. The frequency of HCV viremia increased with the duration of time between diagnosis and sample procurement, and the number of blood products transfused prior to sampling (P = 0.026). No patient who received fewer than 20 U of blood products or who was sampled less than 20 days after diagnosis had a positive HCV RT-PCR result. Of four patients with hepatitis-associated AA (HAAA), one who was sampled 23 days after diagnosis had hepatitis C viremia and a reactive EIA-2 assay. Therefore, the high frequency of HCV viremia in this patient population is most likely due to transfusion with contaminated blood products prior to the introduction of routine blood donor screening for HCV.

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Section: Discussionmentioning

confidence: 98%

Hepatitis C virus infection in acquired aplastic anemia

et al. 1998

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“…Prednisone has been reported to enhance colony formation in some patients with SAA (Bagby et Gorski et al, 1979). However, no in vitro responder could be detected out of five patients who recovered their marrow function after B/6-MPr alone.…”

Section: Discussionmentioning

confidence: 99%

Severe Aplastic Anaemia: Correlation of in Vitro Tests with Clinical Response to Immunosuppression in 20 Patients

et al. 1981

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Colony formation in agar (CFU-c) was studied in 20 patients with severe aplastic anaemia by three different assays: (1) cultures of light density untreated marrow cells; (2) cultures of marrow cells manipulated in order to enhance colony formation (pretreatment with antilymphocytic globulin, ALG, or 6-methylprednisolone, 6-MPr, T cell depletion, adherent cell (AC) depletion, depletion of both AC and T cells), and (3) co-culture of putative suppressor T cells with autologous T-depleted marrow cells. By the first assay, all patients showed poor colony formation (1 +/- 1.5 colonies/10(5) cells; normal controls 46 +/- 18 colonies/10(5) cells). By the second assay, ALG and 6-MPr had no significant effect on colony formation. Removal of adherent cells proved equally without effect on colony growth. On the contrary, removal of T cells enhanced significantly (P less than 0.001) colony formation in 10 out of 20 patients. By the third assay, colony formation of marrow cells (deprived of T lymphocytes) was inhibited by the addition of autologous T cells in six patients studied. All patients were given high dose bolus 6-MPr as first treatment on admission: only patients who had detectable suppressor T cells in their marrow achieved a complete autologous haematologic reconstitution after 6-MPr or after 6-MPr and ALG. The results of this study indicate the detection of CFU-c/suppressor T cells correlates with responses to immunosuppressive regimens, and may thus help to identify patients with immune mediated aplastic anaemia.

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Circulating Suppressor Cells in Aplastic Anemia

Cited by 2 publications

References 5 publications

Hepatitis C virus infection in acquired aplastic anemia

Hepatitis C virus infection in acquired aplastic anemia

Severe Aplastic Anaemia: Correlation of in Vitro Tests with Clinical Response to Immunosuppression in 20 Patients

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