Detection of interleukin-5 messenger RNA in Reed-Sternberg cells of Hodgkin's disease with eosinophilia

Samoszuk, Michael; Nansen, L.

doi:10.1182/blood.v75.1.13.bloodjournal75113

Cited by 16 publications

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“…A few studies have documented the role of cytokine in tumourassociated eosinophilia. IL-5 has been involved in eosinophilia associated with Kumura's (Inoue et al, 1990) and Hodgkin's disease (Samoszuk & Nansen. 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Otherwise, eosinophilia may be due to eosinophilotactic or eosinophilopoietic factors released by tumouractivated T lymphocytes or by the neoplastic cells themselves. Some data support this possibility in carcinomas (Balducci et al 1989: Slungaard et al, 1983, angiolymphoid hyperplasia (Inoue et al, 1990), Hodgkin's disease (Samoszuk & Nansen, 1990). non-Hodgkin lymphomas (Catovsky et al 1980) and some cases of acute lymphoblastic leukaemia (ALL) (Fishel et al 1990).…”

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confidence: 99%

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Role of granulocyte‐macrophage colony‐stimulating factor, Interleukin‐3 and Interleukin‐5 in the eosinophilia associated with T cell lymphoma

et al. 1993

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We studied two patients with a leukaemic T cell lymphoma who presented with a marked increase in blood eosinophilia. To investigate the mechanism of the eosinophilia, supernatants of peripheral blood cells containing more than 80% lymphoma cells were tested by biological assays for the presence of colony stimulating factors (CSF). In one case supernatants stimulated the growth of granulocyte-macrophage (GM), erythroid and eosinophil colonies. These effects were neutralized by anti-GM-CSF antibodies; anti-IL5 antibodies slightly decreased eosinophil colony formation. Supernatants derived from the second patient cells stimulated the same lineages. Neutralizing experiments demonstrated that in addition to GM-CSF it contained interleukin 3 (IL-3) and interleukin 5 (IL-5). In agreement with the biological data, RNA studies using the polymerase chain reaction showed that cells from the first patient expressed GM-CSF transcripts; IL-5 transcripts were also detected in very low amounts. GM-CSF, IL-3 and IL-5 transcripts were detected in cells from the second patient. Thus eosinophilia associated with some T cell lymphoma is likely due to secretion of different combinations of cytokines by malignant cells.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Role of granulocyte‐macrophage colony‐stimulating factor, Interleukin‐3 and Interleukin‐5 in the eosinophilia associated with T cell lymphoma

et al. 1993

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“…Cytokines known to induce signaling via STAT5 associated with members of the IL-2R superfamily are secreted by Hodgkin and Reed-Sternberg (HRS) cells found in Hodgkin's lymphoma (HL) patients. [87][88][89][90] Early reports supported a role for cytokine-driven STAT activation by observing constitutive phosphorylation of STAT1, STAT3, and STAT5 in various T cell lymphomas. 91,92 Additional data supporting a possible connection between STAT5 and lymphoma were provided by Chen et al, who demonstrated that Epstein-Barr virus (EBV) infection, which is associated with multiple malignancies including HL and Burkitt's lymphoma, activates STAT5.…”

Section: Leukemia and Lymphomamentioning

confidence: 99%

The role of STAT5 in the development, function, and transformation of B and T lymphocytes

Heltemes-Harris

Willette

Vang

et al. 2011

Annals of the New York Academy of Sciences

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The transcription factor signal transducer and activator of transcription 5 (STAT5) is activated by a number of cytokine and growth hormone receptors and plays a key role in the development and function of many organ systems. In this review, we focus on recent discoveries about the role of STAT5 in the development and function of B and T lymphocytes. Of particular interest is the growing appreciation for the function of STAT5 as a transcriptional repressor. Finally, we discuss recent discoveries about the role of STAT5 in transformation of B and T lymphocytes.

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“…It was also shown that cultured mast cell line expressed IL-5 mRNA besides 1L-3 and GM-CSF mRNA by cross-linkage of FceRI or upon stimulation with calcium ionophore (49). In human, IL-5 mRNA expression was reported in HTLV-1infected T cells (45), in Reed-Sternberg cells in Hodgkin's disease with eosinophilia (54), and in EB-virus-transformed B cell lines (48).…”

Section: Genes and Structures Of Il-5mentioning

confidence: 98%

Interleukin 5 (IL‐5) and Its Receptor

Takatsu

1991

Microbiology and Immunology

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The antibody response to infectious microbes is regulated by a series of interaction among T cells, B cells, and macrophages. Each B cell is genetically determined to maturate antibody (immunoglobulin, Ig)-producing cells against a distinct antigenic determinant on an infectious microbe, and the antibody produced plays a key role in the Immoral immune response against invading microorganisms. The B cell response to an antigen is regulated by a helper T cell responding to, and specific for, the same antigen molecule. Helper T cells recognize antigenic peptides in context of class II major histocompatibility complex (MHC) molecules on B cells, and secrete several soluble factors which can induce growth and maturation of B cells (23,28,36). IL-5 was initially described as a factor that induces terminal differentiation of already activated murine B cells into Ig-secreting cells and originally designated as T-cell-replacing factor (TRF) (56,65).The establishment of a TRF-producing T-cell hybrid B151K12 (B151) which does not secrete detectable levels of other lymphokines affecting B cells demonstrated that TRF is a lymphokine distinct from IL-1, IL-2, IL-3, IL-4, IL-6, and interferon-gamma (IFN-r) (63, 64). TRF produced by B151 was purified to homogeneity and shown to promote DNA synthesis of murine chronic B cell leukemic cells, BCL1 or of dextran sulfate-stimulated normal B cells, and this activity of TRF is called B-cell growth factor (BCGF) II activity (17, 58).We prepared rat anti-mouse TRF mAb (TB13 and NC17) by using HPLCpurified B151-TRF as irnmunogens (18). Both TB13 and NC17 mAbs blocked biological activity of B151-TRF on B cells and BCL1 cells, whereas they did not inhibit biological activities of other cytokines. B151-TRF was purified by using TB 13-coupled immunoaffinity column and found to have an approximate molecular mass of 46 kDa under nonreducing conditions and of 23 to 26 kDa under reducing conditions on SDS-PAGE analysis, indicating that B151-TRF comprises a dimer form.The molecular cloning of complementary DNA (cDNA) encoding murine TRF has convincingly demonstrated that a single molecule is responsible for both TRF and BCGFII activities (27,42). Although TRF was initially believed to be principally active on B cells, recombinant TRF/BCGFII has been shown to be active on T cells and eosinophil progenitors as well as mature eosinophils (42,66, 77). We therefore proposed that TRF/BCGFII be called 59 3

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Detection of interleukin-5 messenger RNA in Reed-Sternberg cells of Hodgkin's disease with eosinophilia

Cited by 16 publications

References 0 publications

Role of granulocyte‐macrophage colony‐stimulating factor, Interleukin‐3 and Interleukin‐5 in the eosinophilia associated with T cell lymphoma

Role of granulocyte‐macrophage colony‐stimulating factor, Interleukin‐3 and Interleukin‐5 in the eosinophilia associated with T cell lymphoma

The role of STAT5 in the development, function, and transformation of B and T lymphocytes

Interleukin 5 (IL‐5) and Its Receptor

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