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Article: The role of interleukin 13 in classical Hodgkin lymphoma

TitleThe role of interleukin 13 in classical Hodgkin lymphoma
Authors
KeywordsHodgkin lymphoma
Interleukin 13
Autocrine growth factor
STAT6
Issue Date2002
Citation
Leukemia and Lymphoma, 2002, v. 43, n. 6, p. 1203-1210 How to Cite?
AbstractThe Reed-Sternberg (RS) cells of classical Hodgkin lymphoma (cHL) produce several cytokines, which are thought to account for the unique clinical and pathologic features of this disease. We previously identified interleukin (IL)-13 expression as a common feature of cHL and have studied the potential role of this cytokine as an autocrine growth factor for RS cells. IL-13 and the IL-13-specific receptor chain (IL-13Rα1) are frequently expressed in cHL-derived cell lines and in RS cells from biopsies of cHL tissues. In contrast, IL-13 expression in non-Hodgkin lymphoma (NHL) is uncommon. Neutralization of IL-13 in cultures of cHL-derived cell lines HDLM-2 and L-1236 leads to a dose-dependent inhibition of proliferation, and is associated with increased apoptosis in L-1236 cells. IL-13 neutralization also decreased activation of signal transducer and activator of transcription (STAT)6, an important mediator of IL-13 function. Moreover, STAT6 is often activated in RS cells from primary tumor samples, implying that IL-13 signaling is occurring in these cells in vivo. This review will describe the biologic activities of IL-13 in the immune system, and summarize the evidence implicating IL-13 as an autocrine growth factor for RS cells in cHL. Finally, we will discuss the potential influence of IL-13 on the reactive inflammatory infiltrate that is characteristic of cHL.
Persistent Identifierhttp://hdl.handle.net/10722/292515
ISSN
2023 Impact Factor: 2.2
2023 SCImago Journal Rankings: 0.790
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSkinnider, Brian F.-
dc.contributor.authorKapp, Ursula-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:56:38Z-
dc.date.available2020-11-17T14:56:38Z-
dc.date.issued2002-
dc.identifier.citationLeukemia and Lymphoma, 2002, v. 43, n. 6, p. 1203-1210-
dc.identifier.issn1042-8194-
dc.identifier.urihttp://hdl.handle.net/10722/292515-
dc.description.abstractThe Reed-Sternberg (RS) cells of classical Hodgkin lymphoma (cHL) produce several cytokines, which are thought to account for the unique clinical and pathologic features of this disease. We previously identified interleukin (IL)-13 expression as a common feature of cHL and have studied the potential role of this cytokine as an autocrine growth factor for RS cells. IL-13 and the IL-13-specific receptor chain (IL-13Rα1) are frequently expressed in cHL-derived cell lines and in RS cells from biopsies of cHL tissues. In contrast, IL-13 expression in non-Hodgkin lymphoma (NHL) is uncommon. Neutralization of IL-13 in cultures of cHL-derived cell lines HDLM-2 and L-1236 leads to a dose-dependent inhibition of proliferation, and is associated with increased apoptosis in L-1236 cells. IL-13 neutralization also decreased activation of signal transducer and activator of transcription (STAT)6, an important mediator of IL-13 function. Moreover, STAT6 is often activated in RS cells from primary tumor samples, implying that IL-13 signaling is occurring in these cells in vivo. This review will describe the biologic activities of IL-13 in the immune system, and summarize the evidence implicating IL-13 as an autocrine growth factor for RS cells in cHL. Finally, we will discuss the potential influence of IL-13 on the reactive inflammatory infiltrate that is characteristic of cHL.-
dc.languageeng-
dc.relation.ispartofLeukemia and Lymphoma-
dc.subjectHodgkin lymphoma-
dc.subjectInterleukin 13-
dc.subjectAutocrine growth factor-
dc.subjectSTAT6-
dc.titleThe role of interleukin 13 in classical Hodgkin lymphoma-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1080/10428190290026259-
dc.identifier.pmid12152987-
dc.identifier.scopuseid_2-s2.0-0035992266-
dc.identifier.volume43-
dc.identifier.issue6-
dc.identifier.spage1203-
dc.identifier.epage1210-
dc.identifier.isiWOS:000176012600005-
dc.identifier.issnl1026-8022-

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