Decreased CD27 on B Lymphocytes in Patients with Primary Hepatocellular Carcinoma

Xd, Wang; Wang, L; Ji, FJ; Jm, Zhu; Ayana, DA; Fang, XD

doi:10.1177/147323001204000131

Cited by 19 publications

(18 citation statements)

References 26 publications

(30 reference statements)

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“…Multiple mechanisms have been put forward to expli cate the decreased functioning of NK cells and their association with cancer and cirrhosis of the liver, including fibrotic damage to NK cells [30] , phagocytic uptake of NK to B cells during germinal center reactions in secondary lymphoid tissues and function to support Bcell activa tion, affinity maturation, and isotype switching, leading to the generation of memory B cells and longlived plasma cells [39] . Although only a few studies have focused on humoral immunity in HCC and its regulatory mechanisms, impairment of CD4 + Tfh cells has been indicated to influence the development of HBV-associated HCC [40] . A decreased proportion of CXCR5 + CD4 + Tfh cells was found to be associated with HCC disease progression.…”

Section: Nk Cellsmentioning

confidence: 99%

Immunology of hepatocellular carcinoma

Sachdeva

Chawla

Arora

2015

WJH

100

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Hepatocellular carcinoma (HCC) is primarily a malignancy of the liver, advancing from a damaged, cirrhotic liver to HCC. Globally, HCC is the sixth most prevalent cancer and the third-most prevalent reason for neoplastic disease-related deaths. A diverse array of infiltrating immunocytes regulates the development and progression of HCC, as is the case in many other cancers. An understanding of the various immune components during HCC becomes necessary so that novel therapeutic strategies can be designed to combat the disease. A dysregulated immune system (including changes in the number and/or function of immune cells, cytokine levels, and the expression of inhibitory receptors or their ligands) plays a key role in the development of HCC. Alterations in either the innate or adaptive arm of the immune system and cross-talk between them make the immune system tolerant to tumors, leading to disease progression. In this review, we have discussed the status and roles of various immune effector cells (e.g. , dendritic cells, natural killer cells, macrophages, and T cells), their cytokine profile, and the chemokine-receptor axis in promoting or impeding HCC.

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Section: Nk Cellsmentioning

confidence: 99%

Immunology of hepatocellular carcinoma

Sachdeva

Chawla

Arora

2015

WJH

100

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“…A well-studied example of this phenomenon is the cytokine IL-10, a critical Th2 cytokine which blocks the activities of more inflammatory Th1 T-cell cytokines. IL-10 is greatly increased in the serum and tissue of patients with HCC; however, it is not uniformly present in patients with chronic liver disease without HCC, suggesting that IL-10 may be needed for immunosuppression in the established and progressing tumor [118–120]. The chemokine CCL22 also expresses in a similar pattern with IL-10.…”

Section: Non-cellular Factors In the Hbv-associated Hcc Microenvironmentmentioning

confidence: 99%

“…For example, IL-6 plays important roles in tumor initiation but displays a lower level of expression in tumor tissue than in peritumoral tissue [114,115]. However, IL-6 is elevated in the serum of patients with HCC compared to patients with chronic liver disease or healthy controls, and continues to rise as HCC progresses [120–124]. Another example is IL-18, a member of the IL-1 family of cytokines, which has been reported to be present at increasing levels in the serum of patients with HCC compared to patients with cirrhosis or healthy controls [125,126].…”

Section: Non-cellular Factors In the Hbv-associated Hcc Microenvironmentmentioning

confidence: 99%

The hepatitis B virus-associated tumor microenvironment in hepatocellular carcinoma

Yang

Markowitz

Wang

2014

National Science Review

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In contrast to a majority of cancer types, the initiation of hepatocellular carcinoma (HCC) is intimately associated with a chronically diseased liver tissue, with one of the most prevalent etiological factors being hepatitis B virus (HBV). Transformation of the liver in HBV-associated HCC often follows from or accompanies long-term symptoms of chronic hepatitis, inflammation and cirrhosis, and viral load is a strong predictor for both incidence and progression of HCC. Besides aiding in transformation, HBV plays a crucial role in modulating the accumulation and activation of both cellular components of the microenvironment, such as immune cells and fibroblasts, and non-cellular components of the microenvironment, such as cytokines and growth factors, markedly influencing disease progression and prognosis. This review will explore some of these components and mechanisms to demonstrate both underlying themes and the inherent complexity of these interacting systems in the initiation, progression, and metastasis of HBV-positive HCC.

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“…All of these 15 genes mutated in significantly more CRC samples than what expected by chance given the background mutation rate of 1.2×10 –6 (Binomial distribution model, FDR<1%) [59] and 11 of these 15 genes also had copy number deletions in significantly more CRC samples than what expected by random chance given the background copy number alternation rate of 1.2×10 –2 (Binomial distribution model, FDR<1%) [60]. For example, CD53 and CD27 for B cell activation [52], [61] were altered in a total of 45 and 15 CRC patients with somatic mutations or copy number deletions, respectively. Several reverse DE genes, such as CD27, LTF and DOCK2, were also found to be significantly hypermethylated in CRC.…”

Section: Resultsmentioning

confidence: 94%

“…Using the IRIS database, we also found that the UC-CRC inconsistent DE genes were enriched in genes specifically expressed in B cells (P = 0.016). All of the 22 UC-CRC inconsistent DE genes in the “humoral immunity”, including Igα, CD53 and CD27 which play key roles in regulating B-cell activation and immunoglobulin synthesis to mediated humoral immunity [52]–[54], were upregulated in UC but downregulated in CRC, in accordance with the observation that the immune system is hyperactive in UC [55], and that resting B cells can suppress T-cell-mediated anti-tumor immunity in tumors to promote tumor development [56]. Notably, in the “humoral immunity”, there were several DE genes, such as surface receptor CD81 and transmembrane protein LEU13 localizated on B cell membrane surface, that were up-regulated in CRC in comparison with the normal control.…”

Section: Resultsmentioning

confidence: 99%

Functional Comparison between Genes Dysregulated in Ulcerative Colitis and Colorectal Carcinoma

Zhao

Yao

et al. 2013

PLoS ONE

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BackgroundPatients with ulcerative colitis (UC) are predisposed to colitis-associated colorectal cancer (CAC). However, the transcriptional mechanism of the transformation from UC to CAC is not fully understood.MethodologyFirstly, we showed that CAC and non-UC-associated CRC were very similar in gene expression. Secondly, based on multiple datasets for UC and CRC, we extracted differentially expressed (DE) genes in UC and CRC versus normal controls, respectively. Thirdly, we compared the dysregulation directions (upregulation or downregulation) between DE genes of UC and CRC in CRC-related functions overrepresented with the DE genes of CRC, and proposed a regulatory model to explain the CRC-like dysregulation of genes in UC. A case study for “positive regulation of immune system process” was done to reveal the functional implication of DE genes with reversal dysregulations in these two diseases.Principal FindingsIn all the 44 detected CRC-related functions except for “viral transcription”, the dysregulation directions of DE genes in UC were significantly similar with their counterparts in CRC, and such CRC-like dysregulation in UC could be regulated by transcription factors affected by pro-inflammatory stimuli for colitis. A small portion of genes in each CRC-related function were dysregulated in opposite directions in the two diseases. The case study showed that genes related to humoral immunity specifically expressed in B cells tended to be upregulated in UC but downregulated in CRC.ConclusionsThe CRC-like dysregulation of genes in CRC-related functions in UC patients provides hints for understanding the transcriptional basis for UC to CRC transition. A small portion of genes with distinct dysregulation directions in each of the CRC-related functions in the two diseases implicate that their reversal dysregulations might be critical for UC to CRC transition. The cases study indicates that the humoral immune response might be inhibited during the transformation from UC to CRC.

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Decreased CD27 on B Lymphocytes in Patients with Primary Hepatocellular Carcinoma

Abstract: OBJECTIVES: Hepatitis B virus (HBV) replicates in the liver and can lead to hepatocellular carcinoma (HCC

Cited by 19 publications

References 26 publications

Immunology of hepatocellular carcinoma

Immunology of hepatocellular carcinoma

The hepatitis B virus-associated tumor microenvironment in hepatocellular carcinoma

Functional Comparison between Genes Dysregulated in Ulcerative Colitis and Colorectal Carcinoma

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