scholarly journals T gamma (T gamma) cells suppress growth of erythroid colony-forming units in vitro in the pure red cell aplasia of B-cell chronic lymphocytic leukemia.

1982 ◽  
Vol 70 (6) ◽  
pp. 1148-1156 ◽  
Author(s):  
K F Mangan ◽  
G Chikkappa ◽  
P C Farley
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Pure Red Cell Aplasia ◽  
Lymphocytic Leukemia ◽  
Red Cell ◽  
Red Cell Aplasia ◽  
Colony Forming Units ◽  
Cell Chronic Lymphocytic Leukemia

Anti-CD20 monoclonal antibody rituximab for the treatment of B-cell chronic lymphocytic leukemia-associated pure red cell aplasia

2004 ◽  
Vol 5 (6) ◽  
pp. 546-547 ◽  
Author(s):  
Despina Pantelidou ◽  
Costas Tsatalas ◽  
Dimitris Margaritis ◽  
Vasiliki Kaloutsi ◽  
Emmanuel Spanoudakis ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Pure Red Cell Aplasia ◽  
Lymphocytic Leukemia ◽  
Red Cell ◽  
Red Cell Aplasia ◽  
Anti Cd20 ◽  
Cell Chronic Lymphocytic Leukemia

scholarly journals Pure red cell aplasia and hypogammaglobulinemia associated with Tr-cell chronic lymphocytic leukemia

Blood ◽  
1981 ◽  
Vol 57 (6) ◽  
pp. 1025-1031 ◽  
Author(s):  
T Nagasawa ◽  
T Abe ◽  
T Nakagawa
Keyword(s):  
Cell Differentiation ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Colony Formation ◽  
Pure Red Cell Aplasia ◽  
Lymphocytic Leukemia ◽  
Red Cell ◽  
B Cell Differentiation ◽  
Red Cell Aplasia ◽  
Cell Chronic Lymphocytic Leukemia

A 72-yr-old male with Tr-cell chronic lymphocytic leukemia (Tr-CLL) exhibited pure red cell aplasia (PRCA) and hypogammaglobulinemia. During a remission of Tr-CLL, and while receiving cyclophosphamide therapy, he recovered from PRCA and hypogammaglobulinemia. To investigate the pathogenesis of PRCA and hypogammaglobulinemia, we used coculture techniques to study the effect of the malignant Tr cells on erythroid colony formation and B-cell differentiation to immunoglobulin- producing cells. Varying numbers of malignant Tr cells (2 X 10 to 2 X 10(5) cells) were cocultured with 2 X 10(5) normal bone marrow cells. The malignant Tr cells caused a marked reduction of erythroid colony formation in the plasma clot system. This suppression of erythroid colony formation was reversed when the malignant Tr cells were pretreated with antilymphocyte serum and complement. There was no evidence of inhibitory effects in the serum or the supernatant media of the malignant Tr cells stimulated with phytohemagglutinin (PHA). The malignant Tr cells, stored at --80 degrees C before transfusion, were also capable of suppressing autologous erythroid colony formation after recovery from PRCA. In addition, malignant Tr cells were found to have strong suppressor activity against the immunoglobulin biosynthesis by allogeneic B cells. The in vitro suppressions of both erythroid colony formation and B-cell differentiation provide an explanation for the association of PRCA and hypogammaglobulinemia with Tr-CLL.

scholarly journals Pure red cell aplasia and hypogammaglobulinemia associated with Tr-cell chronic lymphocytic leukemia

Blood ◽  
1981 ◽  
Vol 57 (6) ◽  
pp. 1025-1031 ◽  
Author(s):  
T Nagasawa ◽  
T Abe ◽  
T Nakagawa
Keyword(s):  
Cell Differentiation ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Colony Formation ◽  
Pure Red Cell Aplasia ◽  
Lymphocytic Leukemia ◽  
Red Cell ◽  
B Cell Differentiation ◽  
Red Cell Aplasia ◽  
Cell Chronic Lymphocytic Leukemia

Abstract A 72-yr-old male with Tr-cell chronic lymphocytic leukemia (Tr-CLL) exhibited pure red cell aplasia (PRCA) and hypogammaglobulinemia. During a remission of Tr-CLL, and while receiving cyclophosphamide therapy, he recovered from PRCA and hypogammaglobulinemia. To investigate the pathogenesis of PRCA and hypogammaglobulinemia, we used coculture techniques to study the effect of the malignant Tr cells on erythroid colony formation and B-cell differentiation to immunoglobulin- producing cells. Varying numbers of malignant Tr cells (2 X 10 to 2 X 10(5) cells) were cocultured with 2 X 10(5) normal bone marrow cells. The malignant Tr cells caused a marked reduction of erythroid colony formation in the plasma clot system. This suppression of erythroid colony formation was reversed when the malignant Tr cells were pretreated with antilymphocyte serum and complement. There was no evidence of inhibitory effects in the serum or the supernatant media of the malignant Tr cells stimulated with phytohemagglutinin (PHA). The malignant Tr cells, stored at --80 degrees C before transfusion, were also capable of suppressing autologous erythroid colony formation after recovery from PRCA. In addition, malignant Tr cells were found to have strong suppressor activity against the immunoglobulin biosynthesis by allogeneic B cells. The in vitro suppressions of both erythroid colony formation and B-cell differentiation provide an explanation for the association of PRCA and hypogammaglobulinemia with Tr-CLL.

scholarly journals Difficulties of anemia diagnosis in patients with B-cell chronic lymphocytic leukemia

2021 ◽  
Vol 16 (2) ◽  
pp. 40-47
Author(s):  
I. S. Piskunova ◽  
T. N. Moiseeva ◽  
L. S. Al-Radi ◽  
L. V. Plastinina ◽  
S. R. Goryacheva
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Immune Thrombocytopenia ◽  
Lymphocytic Leukemia ◽  
Red Cell ◽  
Red Cell Aplasia ◽  
Cell Chronic Lymphocytic Leukemia

Cytopenia commonly occurs in case of chronic lymphocytic leukemia. It can either precede the diagnosis of chronic lymphocytic leukemia or appear at any time during the disease. Autoimmune hemolytic anemia, immune thrombocytopenia, and partial red cell aplasia are most often found among cytopenias in chronic lymphocytic leukemia. At the same time, the development of cytopenia may be associated with the displacement of normal hematopoiesis cells by tumor lymphocytes. It is very important to accurately diagnose and identify the cause of cytopenia in chronic lymphocytic leukemia, since the prognosis and therapy differ significantly.

scholarly journals Defective T cell-mediated, isotype-specific immunoglobulin regulation in B cell chronic lymphocytic leukemia

Blood ◽  
1988 ◽  
Vol 71 (4) ◽  
pp. 1012-1020 ◽  
Author(s):  
JS Moore ◽  
MB Prystowsky ◽  
RG Hoover ◽  
EC Besa ◽  
PC Nowell
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Cell Activity ◽  
Lymphocytic Leukemia ◽  
Specific Immunoglobulin ◽  
Cell Chronic Lymphocytic Leukemia

The consistent occurrence of T cell abnormalities in patients with B cell chronic lymphocytic leukemia (B-CLL) suggest that the non- neoplastic host T cells may be involved in the pathogenesis of this B cell neoplasm. Because potential defects of immunoglobulin regulation are evident in B-CLL patients, we investigated one aspect of this by studying the T cell-mediated immunoglobulin isotype-specific immunoregulatory circuit in B-CLL. The existence of class-specific immunoglobulin regulatory mechanisms mediated by Fc receptor-bearing T cells (FcR + T) through soluble immunoglobulin binding factors (IgBFs) has been well established in many experimental systems. IgBFs can both suppress and enhance B cell activity in an isotype-specific manner. We investigated the apparently abnormal IgA regulation in a B-CLL patient (CLL249) whose B cells secrete primarily IgA in vitro. Enumeration of FcR + T cells showed a disproportionate increase in IgA FcR + T cells in the peripheral blood of this patient. Our studies showed that the neoplastic B cells were not intrinsically unresponsive to the suppressing component of IgABF produced from normal T cells, but rather the IgABF produced by the CLL249 host T cells was defective. CLL249 IgABF was unable to suppress IgA secretion by host or normal B cells and enhanced the in vitro proliferation of the host B cells. Size fractionation of both normal and CLL249 IgABF by gel-filtration high- performance liquid chromatography (HPLC) demonstrated differences in the ultraviolet-absorbing components of IgABF obtained from normal T cells v that from our patient with defective IgA regulation. Such T cell dysfunction may not be restricted to IgA regulation, since we have found similar expansion of isotype-specific FcR + T cells associated with expansion of the corresponding B cell clone in other patients with B-CLL. These data suggest that this T cell-mediated regulatory circuit could be significantly involved in the pathogenesis of B-CLL.

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