Rituximab or irradiation promotes IL-17 secretion and thereby induces resistance to rituximab or irradiation

Zhong, Weide; Liu, Qingshan

doi:10.1038/cmi.2017.124

Cited by 16 publications

(24 citation statements)

References 15 publications

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“…To further investigate the signaling pathways involved in the function of IL-6 and IL-17A in DLBCL cells, we performed microarray analysis, western blotting, and qPCR. Recent studies from our group showed that IL-17A promotes DLBCL cell growth by suppressing p53 expression [17, 18]. In the present study, microarray analysis showed that IL-17A decreased the activity of the p53 pathway (Fig.…”

Section: Discussionsupporting

confidence: 64%

Human bone marrow-derived mesenchymal stem cells promote the growth and drug-resistance of diffuse large B-cell lymphoma by secreting IL-6 and elevating IL-17A levels

Zhong

Zhu

et al. 2019

J Exp Clin Cancer Res

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BackgroundThe drug-resistance and relapse of diffuse large B-cell lymphoma (DLBCL), which are related to mesenchymal stem cells (MSCs), have become increasingly common. However, the underlying mechanisms remain elusive.MethodsCCK 8 assay, colony formation assay, and xenograft mouse model were used to investigate the effects of hBMSCs on DLBCL growth. Immunohistochemistry, qRT-PCR, and ELISA were used to study the expressions of IL-6 and IL-17A. Flow cytometry was used to analyze Th17 cells and Treg cells expressions. Western blot analysis, microarray analysis, and bioinformatics analysis were used to analyze the pathways of IL-6 or IL-17A mediated DLBCL growth.ResultsHBMSCs promoted DLBCL growth by secreting IL-6 in vitro and in vivo and simultaneously upregulating IL-17A in vitro. IL-6 and IL-17A synergistically promoted the growth and drug-resistance of DLBCL cells by protecting them from spontaneous or drug-induced apoptosis in vitro. IL-6 or IL-17A activated the JAK2/STAT3 pathway or upregulated cyclin D2 via activation of PI3K/Akt signaling in vitro, respectively.ConclusionsThe present results indicated that hBMSCs might have a “dual effect” on promoting DLBCL progression and drug-resistance by secreting IL-6 and upregulating IL-17A. IL-6, IL-17A, p-STAT3, p-Akt or cyclin D2 may be potential molecular targets for overcoming drug-resistance in patients with relapsed or refractory DLBCL.

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Section: Discussionsupporting

confidence: 64%

Human bone marrow-derived mesenchymal stem cells promote the growth and drug-resistance of diffuse large B-cell lymphoma by secreting IL-6 and elevating IL-17A levels

Zhong

Zhu

et al. 2019

J Exp Clin Cancer Res

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“…Rituximab has been shown to be effective in some autoimmune diseases, so the question remains as to why it is neither clinically effective in the treatment of AIH nor in the emAIH model. Among the molecules and presented mechanisms, IL-17 was shown to be expressed after rituximab administration [53]. Therefore, we suggest that anti-CD20 therapy should be combined with complexed, low-dose anti-IL-2 therapy, adoptive Treg transfer, or both [20,54].…”

Section: Discussionmentioning

confidence: 95%

Anti-CD20 Therapy Alters the Protein Signature in Experimental Murine AIH, but Not Exclusively towards Regeneration

Buitrago‐Molina

Dywicki

Noyan

et al. 2021

Cells

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Background: Autoimmune hepatitis (AIH) is a chronic autoimmune inflammatory disease that usually requires lifelong immunosuppression. Frequent recurrences after the discontinuation of therapy indicate that intrahepatic immune regulation is not restored by current treatments. Studies of other autoimmune diseases suggest that temporary depletion of B cells can improve disease progression in the long term. Methods: We tested a single administration of anti-CD20 antibodies to reduce B cells and the amount of IgG to induce intrahepatic immune tolerance. We used our experimental murine AIH (emAIH) model and treated the mice with anti-CD20 during the late stage of the disease. Results: After treatment, the mice showed the expected reductions in B cells and serum IgGs, but no improvements in pathology. However, all treated animals showed a highly altered serum protein expression pattern, which was a balance between inflammation and regeneration. Conclusions: In conclusion, anti-CD20 therapy did not produce clinically measurable results because it triggered inflammation, as well as regeneration, at the proteomic level. This finding suggests that anti-CD20 is ineffective as a sole treatment for AIH or emAIH.

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“…Activation of PKC by IL-17 is associated with enhanced PKC ability to regulate cell cycle progression in leukemia cells [130]. As indicated earlier, IL-17 is profoundly implicated in many human diseases [55][56][57][58][59][60][61][62][63][64][65][66][67][68][69][70][71][72][73][74], thus supporting the suggestion that design and production of anti-IL-17 drugs could lead to better strategies for development of new therapies for those diseases [88][89][90]. Although the recent reports implicating IL-17 in the mechanism of the "cytokine storm" event in COVID-19 infection is far from conclusion, there are calls for development of anti-IL-17 drugs as adjunct therapy for diseases in which IL-17 plays an active role [87,131].…”

Section: Discussionmentioning

confidence: 99%

“…Clinically, IL-17 is implicated in numerous diseases including arthritis [52][53][54], classical Hodgkin lymphomas [55][56][57], multiple myeloma [58][59][60], airway diseases including asthma [61,62], musculoskeletal diseases [63,64], inflammatory bowel diseases (IBDs) [65] autoimmune diseases [66], and different types of cancer [67][68][69]. Significantly elevated level of IL-17 and IL-17R are found in these diseases and IL-17 and IL-17R are known to promote anti-apoptotic effects and survival mechanisms in some types of cancer [55][56][57][58][59][60][61][62][63][64][65][66]. In most cases, IL-17 itself and/or IL-17dependent cytokines produced downstream of the IL-17R, contribute to various pathological conditions associated with these diseases [55][56][57][58][59][60][61][62][63][64][65][66][67][68].…”

Section: Introductionmentioning

confidence: 99%

“…Significantly elevated level of IL-17 and IL-17R are found in these diseases and IL-17 and IL-17R are known to promote anti-apoptotic effects and survival mechanisms in some types of cancer [55][56][57][58][59][60][61][62][63][64][65][66]. In most cases, IL-17 itself and/or IL-17dependent cytokines produced downstream of the IL-17R, contribute to various pathological conditions associated with these diseases [55][56][57][58][59][60][61][62][63][64][65][66][67][68]. Furthermore, Hox3/ IL-17R expression ratio has been implicated in poor prognosis in some breast cancer patients undergoing tamoxifen chemotherapy as IL-17 promotes resistance to chemotherapy in breast cancer [67][68][69][70][71].…”

Section: Introductionmentioning

confidence: 99%

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IL-17 Biological Effects and Signaling Mechanisms in Human Leukemia U937 Cells

Adunyah¹,

Akomeah²,

Arthur³

et al. 2021

Interleukins - The Immune and Non-Immune Systems’ Related Cytokines

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Human Interlekin-17 is produced by memory activated CD4+ T cells and other cells. It was initially considered unique in that its specific receptor is distinct from other cytokine receptors. IL-17 receptor is ubiquitously expressed by different cells including T cells. IL-17 plays a role in regulating growth, immune response and pro-inflammatory responses. It regulates differentiation of a subset of Th0 cells into Th-17 cells, which produce IL-17-induced cytokines. The IL-17R belongs to type 1 cytokine receptors. IL-17 belongs to a superfamily of its own, which includes IL-17A, IL-17B, IL-17C, IL-17E and IL-17F. These members of IL-17 superfamily have some sequence homology but bind to different receptors. Prior to this investigation, limited information existed on the effects of IL-17A in human leukemia cell lines. Our results show that IL-17A promotes growth, anti-apoptotic effects, chemotaxis, cytokine expression and transcriptional factor activation in leukemia cells. IL-17A activates multiple signaling pathways including PI-3 K, Jak–STAT, Raf-ERK1/2 and SRC kinase pathways, which mediate different biological effects of IL-17A in leukemia cells. Our findings implicate IL-17A in leukemia cell growth and survival, supporting potential leukemia therapy via development of anti-IL-17A drugs. This chapter focuses on IL-17A, herein referred to as IL-17.

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Rituximab or irradiation promotes IL-17 secretion and thereby induces resistance to rituximab or irradiation

Cited by 16 publications

References 15 publications

Human bone marrow-derived mesenchymal stem cells promote the growth and drug-resistance of diffuse large B-cell lymphoma by secreting IL-6 and elevating IL-17A levels

Human bone marrow-derived mesenchymal stem cells promote the growth and drug-resistance of diffuse large B-cell lymphoma by secreting IL-6 and elevating IL-17A levels

Anti-CD20 Therapy Alters the Protein Signature in Experimental Murine AIH, but Not Exclusively towards Regeneration

IL-17 Biological Effects and Signaling Mechanisms in Human Leukemia U937 Cells

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