Cytosine–phosphate–guanosine-DNA induces CD274 expression in human B cells and suppresses T helper type 2 cytokine production in pollen antigen-stimulated CD4-positive cells

Kubo, Shigeru; Yamada, Tetsuji; Osawa, Yusuke; Ito, Yatsuji; Narita, Norihiko; Fujieda, Shigeharu

doi:10.1111/j.1365-2249.2012.04585.x

Cited by 18 publications

(14 citation statements)

References 27 publications

(43 reference statements)

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“…Previous studies have reported that CD274 exerts its effects on tumors through the regulation of tumor immunity. For example, CD274 suppresses type 1 T helper cell-based immune responses and induces T cell apoptosis in vitro via the inhibitory receptor programmed cell death protein 1, which aids the escape of tumor cells from the immune system (32,33). The present study demonstrated that the expression levels of CD274 in LSCC were positively correlated with the TNM stage of cancer, lymph node metastasis and the pathological stage of cancer.…”

Section: Discussionsupporting

confidence: 53%

Competing endogenous RNA network analysis of CD274, IL‑10 and FOXP3 co‑expression in laryngeal squamous cell carcinoma

et al. 2017

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Laryngeal squamous cell carcinoma (LSCC) is one of the most common types of head and neck malignant tumor; however, there is a lack of effective molecular targets for therapy. The present study detected the expression of three immunity‑associated molecules [forkhead box (FOX)3, interleukin (IL)‑10 and cluster of differentiation (CD)274] in 133 LSCC samples using immunohistochemistry (IHC); subsequently, the association between their expression and the clinical characteristics of LSCC were analyzed. Spearman's rank correlation method, Kaplan‑Meier and Cox regression model were used to analyze the correlations of the three proteins and their clinical significance. StarBase and miRTarBase databases were used to establish the competitive endogenous (ce)RNA network of the three molecules. IHC demonstrated that the positive expression rates of FOXP3, IL‑10 and CD274 were 68.4, 73.7 and 58.6% in 133 LSCC samples, respectively. In addition, it was identified that the expression of the three proteins was closely correlated with the clinical characteristics of LSCC, including lymph node metastasis and prognosis (P<0.05). There was also a significant association of co‑expression between any two proteins (P<0.001). Furthermore, the expression levels of FOXP3, IL‑10 and CD274 were negatively associated with the survival rate of patients with LSCC (P<0.05). The results of a Cox regression model suggested that the three proteins were prognostic risk factors for LSCC (P<0.05). The ceRNA network revealed that 10 microRNAs (miRs; including miR‑16‑5p and miR‑214‑3p), 123 long non‑coding RNAs (including X‑inactive specific transcript, H19 and metastasis associated lung adenocarcinoma transcript 1) and 408 circular RNAs (including ATP‑binding cassette subfamily C member 1 hsa_circ_001569 and ISY1 splicing factor homolog hsa_circ_001859) may regulate the expression of FOXP3, IL‑10 and CD274. The data generated from the present study may increase the understanding of the immune escape mechanisms of LSCC and may be beneficial for the development of a specific immunotherapy.

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Section: Discussionsupporting

confidence: 53%

Competing endogenous RNA network analysis of CD274, IL‑10 and FOXP3 co‑expression in laryngeal squamous cell carcinoma

et al. 2017

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“…Next, we asked whether the decrease in the frequency of PD-L1 + B cells in RA patients was due to an intrinsic defect of the B cells from these patients to express this molecule, or whether these B cells could upregulate PD-L1 under certain stimuli. PD-L1 increases when purified human B cells are incubated with CpG nucleotides ( 18 , 36 ). To determine the ability of CD19 + B cells from untreated RA patients to upregulate PD-L1, we purified CD19 + B cells from PBMC of untreated RA patients and incubated them during 72 h with medium alone or with CpG+IL-2.…”

Section: Resultsmentioning

confidence: 99%

“…B cells and plasmablasts can also modulate the T cell immune response through the expression of regulatory molecules, such as PD-L1 ( 16 , 17 ). CpG induces PD-L1 expression on human B cells, which suppresses T helper type 2 cytokine production in pollen antigen-stimulated CD4-positive cells ( 18 ). Tumor-infiltrating IgA + B cells that express high levels of PD-L1, IL-10 and TGF-β repress the proliferation and activation of CD8 + T cells ( 19 ).…”

Section: Introductionmentioning

confidence: 99%

PD-L1+ Regulatory B Cells Are Significantly Decreased in Rheumatoid Arthritis Patients and Increase After Successful Treatment

et al. 2018

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Background: B cells play an important role in the development and maintenance of rheumatoid arthritis (RA). Although IL-10–producing B cells represent a major subset of regulatory B cells (Bregs) able to suppress autoimmune and inflammatory responses, recent reports showed that B cell-mediated immune suppression may also occur independent of IL-10. For instance, B cells can modulate T cell immune responses through the expression of regulatory molecules such as PD-L1. So far, PD-L1-expressing B cells have not been analyzed in RA patients.Objective: To analyze the frequency of PD-L1-expressing B cells in the peripheral blood of RA patients compared to healthy controls (HC) matched for sex and age, their function on T cell response and their changes in response to therapy.Methods: Fresh peripheral blood B cells from RA patients and HC were characterized by flow cytometry and their functionality assessed in a co-culture system with autologous T cells.Results: The frequencies of CD19+PD-L1+ B cells, CD24hiCD38−PD-L1+ and CD24hiCD38hiPD-L1+ B cells were significantly lower in untreated RA patients than in HC. In a follow-up study, the frequencies of PD-L1+ B cells (CD19+PD-L1+ B cells, CD24hiCD38−PD-L1+ and CD24hiCD38hiPD-L1+ B cells) increased significantly after treatment in good responder patients, although the frequency of total CD24hiCD38hi B cells decreased. CD19+ B cells from untreated RA patients and HC upregulated PD-L1 expression similarly upon stimulation with CpG plus IL-2 and were able to suppress, in vitro, CD8+ T cell proliferation and cytokine production in a PD-L1-dependent manner.Conclusions: Our results show that PD-L1+ B cells exhibiting T cell suppressive capacity are significantly decreased in untreated RA patients but increase in response to successful treatment. PD-L1 expression on B cells from RA patients can be modulated in vitro and PD-L1+ B cells could thus provide new perspectives for future treatment strategies.

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“…It is important to know the cellular source, either paracrine or autocrine, of the PD-1 ligands (PD-L1 and PD-L2). In this regard, PD-L1 can be induced in human B cells after stimulation with CpG-DNA, a TLR9 agonist, in vitro [49].…”

Section: Redistribution Of Classic and Rare Populations Of Memory B Cmentioning

confidence: 99%

Impairment of B-cell functions during HIV-1 infection

Amu

Ruffin

Réthi

et al. 2013

Aids

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A variety of B-cell dysfunctions are manifested during HIV-1 infection, as reported early during the HIV-1 epidemic. It is not unusual that the pathogenic mechanisms presented to elucidate impairment of B-cell responses during HIV-1 infection focus on the impact of reduced T-cell numbers and functions, and lack of germinal center formation in lymphoid tissues. To our understanding, however, perturbation of B-cell phenotype and function during HIV-1 infection may begin at several different B-cell developmental stages. These impairments can be mediated by intrinsic B-cell defects as well as by the lack of proper T-cell help. In this review, we will highlight some of the pathways and molecular interactions leading to B-cell impairment prior to germinal center formation and B-cell activation mediated through the B-cell receptor in response to HIV-1 antigens. Recent studies indicate a regulatory role for B cells on T-cell biology and immune responses. We will discuss some of these novel findings and how these regulatory mechanisms could potentially be affected by the intrinsic defects of B cells taking place during HIV-1 infection.

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Cytosine–phosphate–guanosine-DNA induces CD274 expression in human B cells and suppresses T helper type 2 cytokine production in pollen antigen-stimulated CD4-positive cells

Cited by 18 publications

References 27 publications

Competing endogenous RNA network analysis of CD274, IL‑10 and FOXP3 co‑expression in laryngeal squamous cell carcinoma

Competing endogenous RNA network analysis of CD274, IL‑10 and FOXP3 co‑expression in laryngeal squamous cell carcinoma

PD-L1+ Regulatory B Cells Are Significantly Decreased in Rheumatoid Arthritis Patients and Increase After Successful Treatment

Impairment of B-cell functions during HIV-1 infection

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