Differential Effect of IL-4 and IL-13 on CD44 Expression in the Burkitt's Lymphoma B Cell Line BL30/B95-8 and in Epstein–Barr Virus (EBV) Transformed Human B Cells: Loss of IL-13 Receptors on Burkitt's Lymphoma B Cells

Gee, Katrina; Kozlowski, Maya; Kryworuchko, Marko; Díaz‐Mitoma, Francisco; Kumar, Ashok

doi:10.1006/cimm.2001.1829

Cited by 19 publications

(16 citation statements)

References 53 publications

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Section: Discussionmentioning

confidence: 88%

“…The unresponsiveness of the BL lines to IL-13 is in line with the fact that they do not express the IL-13R␣1. 41 Furthermore, we found that the type III EBV gene expression leads to the down-regulation of IL-4R␣ expression, as evidenced by the isogenic type I/type III BL lines Mutu and Jijoye.In our previous publication 17 LMP-1 was induced by CD40L and IL-4 in the KMH2-EBV cells. Presently, we have found that CD40L is dispensable for this effect in the KMH2-EBV cells.…”

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confidence: 88%

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STAT6 signaling pathway activated by the cytokines IL-4 and IL-13 induces expression of the Epstein-Barr virus–encoded protein LMP-1 in absence of EBNA-2: implications for the type II EBV latent gene expression in Hodgkin lymphoma

Kis

Gerasimčik

Salamon

et al. 2011

Blood

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IntroductionEpstein-Barr virus (EBV) is a ␥-herpes virus of the Lymphocryptovirus genus that has succeeded to colonize Ͼ 90% of the adult population. 1 As a general characteristic of these viruses, they can all infect and immortalize B-lymphocytes in vitro. The in vitro EBV-infected B cells proliferate and give rise to lymphoblastoid cell lines (LCLs). The pattern of latent EBV gene expression seen in LCLs is referred to as the type III latency, in which 9 virally encoded proteins are expressed (EBV nuclear antigen 1-6 [EBNA1-6], Latent Membrane Protein-1 [LMP-1], LMP-2A, and LMP-2B). 1 Similarly to the EBV gene expression seen in LCLs, type III latent B cells were found in healthy persons during the primary infection 2 and the virus carrier state. 3 These cells are highly immunogenic and are eliminated by the cellular immune response. 4 After the primary infection the virus establishes a life-long infection in the memory B-cell reservoir, from where it is thought to reactivate and produce new progeny that are shed in the saliva. 1,5 In immunodeficient states, in which the cellular immune responses are compromised, the EBV-infected type III B cells can give rise to lymphoproliferations/lymphomas, as seen in the posttransplantation lymphoproliferations 6,7 and some AIDS lymphomas. 8 Depending on the histologic origin, the activation state, and the differentiation stage of the virus-carrying cells, EBV can adopt other viral gene expression patterns as well. 9 This is evidenced by the type I EBV gene expression seen in Burkitt lymphomas (BLs), primary effusion lymphomas, 10 and diffuse large B-cell lymphomas, whereby EBNA-1 is the only viral protein expressed. However, EBNA-1 is coexpressed with LMP-1 and LMP-2 in the EBV-carrying classical HL (cHL 11 ; type II latency), nasal natural killer/T-cell lymphoma, 12,13 some nasopharyngeal carcinomas (NPCs), 14,15 and peripheral T-cell lymphomas. 16 The expression of LMP-1 in type III latency is driven by the EBNA-2 protein. 1 The molecular mechanism of LMP-1 expression in type II latent cells, thus in the absence of EBNA-2, is only partially known. EBV-positive cHL is unique among the type II malignancies because all the Hodgkin/Reed-Sternberg (HRS) cells express high levels of LMP-1, whereas LMP-1 expression is heterogeneous in other tumors. 15 Not just the mechanism of LMP-1 expression in the HRS cells is unknown, but it is still an open question whether LMP-1 is needed for the survival or proliferation of these malignant cells. Although the type II EBV latency is seen in a proportion of cHLs, the available HL-derived cell lines are EBV negative. Thus, there is no in vitro system in which this type of virus-cell interaction can be studied.We have previously reported that exposure of the in vitro EBV-converted HL-derived cell line KMH2-EBV to CD40 ligand (CD40L) and interleukin-4 (IL-4) led to EBNA-2-independent expression of LMP-1. 17 In the continuation of this work we identify now IL-4, IL-13, and CD40L as potent inducers of LMP-1 not only Submitted January 21, 2010...

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Section: Discussionmentioning

confidence: 88%

mentioning

confidence: 88%

STAT6 signaling pathway activated by the cytokines IL-4 and IL-13 induces expression of the Epstein-Barr virus–encoded protein LMP-1 in absence of EBNA-2: implications for the type II EBV latent gene expression in Hodgkin lymphoma

Kis

Gerasimčik

Salamon

et al. 2011

Blood

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“…While expressing STAT6, the DLBCL cell lines did not show any evidence of STAT6 phosphorylation. STAT6 phosphorylation in MedB1 cells was also detected in cells grown in serum-free medium (data not shown) and was further enhanced by IL-4 or IL-13 treatment, while only IL-4 induced P-STAT6 in Ramos cells, because of the absence of IL-13␣1 receptor in Burkitt-derived cells 22 ( Figure 2B). …”

Section: Stat6 Activation In Pmbl-derived Cell Linesmentioning

confidence: 82%

Constitutive STAT6 activation in primary mediastinal large B-cell lymphoma

Guiter

Dusanter‐Fourt

Copie‐Bergman

et al. 2004

Blood

178

124

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“…Phosphorylation of p38, p42/44, and JNK MAPKs was determined by Western blot analysis using MAPK-specific Abs as previously described (30,35,36). Cells were stimulated at 37°C for 0 -15 min with either LPS, IL-10, or TNF-␣.…”

Section: Western Blot Analysismentioning

confidence: 99%

Differential Regulation of CD44 Expression by Lipopolysaccharide (LPS) and TNF-α in Human Monocytic Cells: Distinct Involvement of c-Jun N-Terminal Kinase in LPS-Induced CD44 Expression

Gee

Lim

et al. 2002

The Journal of Immunology

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Alterations in the regulation of CD44 expression play a critical role in modulating cell adhesion, migration, and inflammation. LPS, a bacterial cell wall component, regulates CD44 expression and may modulate CD44-mediated biological effects in monocytic cells during inflammation and immune responses. In this study, we show that in normal human monocytes, LPS and LPS-induced cytokines IL-10 and TNF-α enhance CD44 expression. To delineate the mechanism underlying LPS-induced CD44 expression, we investigated the role of the mitogen-activated protein kinases (MAPKs), p38, p42/44 extracellular signal-regulated kinase, and c-Jun N-terminal kinase (JNK) by using their specific inhibitors. We demonstrate the involvement, at least in part, of p38 MAPK in TNF-α-induced CD44 expression in both monocytes and promonocytic THP-1 cells. However, neither p38 nor p42/44 MAPKs were involved in IL-10-induced CD44 expression in monocytes. To further dissect the TNF-α and LPS-induced signaling pathways regulating CD44 expression independent of IL-10-mediated effects, we used IL-10 refractory THP-1 cells as a model system. Herein, we show that CD44 expression induced by the LPS-mediated pathway predominantly involved JNK activation. This conclusion was based on results derived by transfection of THP-1 cells with a dominant-negative mutant of stress-activated protein/extracellular signal-regulated kinase kinase 1, and by exposure of cells to JNK inhibitors dexamethasone and SP600125. All these treatments prevented CD44 induction in LPS-stimulated, but not in TNF-α-stimulated, THP-1 cells. Furthermore, we show that CD44 induction may involve JNK-dependent early growth response gene activation in LPS-stimulated monocytic cells. Taken together, these results suggest a predominant role of JNK in LPS-induced CD44 expression in monocytic cells.

show abstract

Differential Effect of IL-4 and IL-13 on CD44 Expression in the Burkitt's Lymphoma B Cell Line BL30/B95-8 and in Epstein–Barr Virus (EBV) Transformed Human B Cells: Loss of IL-13 Receptors on Burkitt's Lymphoma B Cells

Cited by 19 publications

References 53 publications

STAT6 signaling pathway activated by the cytokines IL-4 and IL-13 induces expression of the Epstein-Barr virus–encoded protein LMP-1 in absence of EBNA-2: implications for the type II EBV latent gene expression in Hodgkin lymphoma

STAT6 signaling pathway activated by the cytokines IL-4 and IL-13 induces expression of the Epstein-Barr virus–encoded protein LMP-1 in absence of EBNA-2: implications for the type II EBV latent gene expression in Hodgkin lymphoma

Constitutive STAT6 activation in primary mediastinal large B-cell lymphoma

Differential Regulation of CD44 Expression by Lipopolysaccharide (LPS) and TNF-α in Human Monocytic Cells: Distinct Involvement of c-Jun N-Terminal Kinase in LPS-Induced CD44 Expression

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