Background: Prostate cancer spans a broad spectrum from indolent to deadly disease. In the management of prostate cancer, diagnostic biopsy specimens are important sources of data that inform the selection of treatment. B7-H3 (CD276), an immune checkpoint molecule, has emerged as a promising immunotherapy target. B7-H3 expression is related to adverse clinical outcomes in various types of cancer; however, little is known concerning the association between tumor B7-H3 expression in diagnostic biopsy specimens and clinical outcome in patients with metastatic prostate cancer.

Methods: We evaluated tumor B7-H3 expression levels in diagnostic biopsy specimens from 135 patients with metastatic prostate cancer and 113 patients with localized prostate cancer.

Results: High B7-H3 expression was more frequently observed in patients with metastatic cancer than in those with localized cancer (31 vs. 12%; p = 0.0003). In patients with localized cancer, the B7-H3 expression status was not associated with biochemical recurrence-free survival. However, among patients with metastatic cancer, high B7-H3 expression was independently associated with high disease-specific mortality (multivariable hazard ratio [HR] = 2.72; p = 0.047) and overall mortality rates (multivariable HR = 2.04; p = 0.025).

Conclusions: Tumor B7-H3 expression in diagnostic biopsy specimens may be a useful biomarker for identifying highly aggressive metastatic prostate cancer. Given the potential utility of anti-B7-H3 immunotherapy, this information may aid in stratifying prostate cancer based on its responsiveness to B7-H3-targeted treatment.

Acute Myeloid Leukaemia (AML) is a neoplasia characterised by rapid proliferation and an increased rate of relapses. The AML blasts display features of antigen-presenting cells (APC), and thus can directly modulate the anti-tumour T cell responses. The bone marrow of a group consisting of 30 newly diagnosed patients and four healthy donors (HD) was investigated for the expression of HLA-DR, several molecules involved in MHC-II antigen-presentation and MHC-II groove editing, like HLA-DM, CD74 and CLIP, as well as a set of immune checkpoint ligands, like ICOS-L, B7.2, PD-L2 and B7-H3. The patients were further characterised for their genetic anomalies and distributed to favourable, intermediate and adverse ELN risk categories. We were able to show that while 23% of our patients displayed a low level of HLA-DR surface expression, all patients displayed higher HLA-DM and CD74 expression compared to HD. However, a higher CLIP expression was noticed only in the HLA-DR low patients. The co-inhibitory PD-L2 and B7-H3 molecules were increased in the cases with normal HLA-DR expression; oppositely, the co-stimulatory ICOS-L and the dual function B7.2 were significantly increased in the cases with HLA-DR low expression. Furthermore, no favourable ELN risk cases were found within the HLA-DR low group. All in all, these data show that the AML with low versus normal HLA-DR expression display different profiles of MHC class II machinery molecules and B7 ligands, which are correlated with distinct ELN stratification. Furthermore, as our study included healthy individuals, it offers valuable information about the expression levels that should be considered as normal for these markers known to cause differences in peptide repertoires, reflected further in distinct T-cells polarisation pathways.

Keywords: AML; Antigen-presentation; HLA; HLA-DM; Immunotherapy; Invariant chain.

At present, there are no widely accepted specific biomarkers for the experimental diagnosis of chronic prostatitis / chronic pelvic pain syndrome (CP/CPPS). Recent studies show that many related biomarkers exist in expressed prostatic secretions (EPS) or semen, urine and blood or serum. The monocyte chemotactic protein-1 (MCP-1/CCL-2), macrophage-inflammatory-protein-1 alpha (MIP-1α/CCL-3), interleukin-6 (IL-6), interleukin-8 (IL-8), nerve growth factor (NGF) and B7-H3 in EPS, prostatic exosomal protein (PSEP) in the urine, and prostate-specific antigen (PSA), mean platelet volume (MPV) and macrophage migration inhibitory factor (MIF) in the serum are believed to be of significant clinical and research value, and expected to become important laboratory biomarkers for the diagnosis of CP/CPPS.

Keywords: biomarker; experimental diagnosis; expressed prostatic secretion; chronic prostatitis / chronic pelvic pain syndrome.

Ethidium bromide (EtBr) is an intercalating agent, which binds tightly to mitochondrial DNA (mtDNA) during replication, and so blocks the function of mitochondria. EtBr inserts itself between the stacked bases in double-stranded DNA and specifically inhibits mtDNA transcription and replication by deleting RNA primers required for initiating mtDNA replication. In this study, the authors wanted to examine whether blocking mtDNA replication with EtBr could change the expression of stenmness genes and the expression of the immuneregulator B7-H3 in prostate cancer cell lines in vitro. Both PC-3 and DU145 prostate cancer cell lines were treated with 50 and 500 ng/mL of EtBr for 2 weeks. There was no difference in growth between EtBr-treated and control cells after 1 week. A slightly slower growth was observed for both cell lines during the second week of culture with EtBr compared to controls. After 2 weeks of culture with EtBr both cell lines showed increased expression of the stemness-related genes ABCG2, Oct3/4, Nanog1/Nanogp8, and CD44. Concomitantly, a dose-dependent increase of B7-H3 protein expression in both cell lines was identified and verified by both flow cytometry and immunocytochemistry. In conclusion, blocking mtDNA replication by EtBr induces increased expression of stemness genes, such as Oct3/4, Nanog, CD44, and ABCG2, in addition to the immune regulator B7-H3 in PC-3 and DU145 prostate cancer cell lines. The findings indicate that mitochondrial function may be associated with stemness of cancer cells and/or maintenance of a cancer stem cell phenotype. The finding of increased B7-H3 expression may be associated with the immunosuppression of cancer cells.

OBJECTIVE

Co-signaling molecules PD-L1, B7-H3, and PD-1 play a key role in cancer immunology. There are limited but emerging data on expression of these molecules in HIV-infected lung cancer patients.

METHODS

We reviewed archived lung cancer tissue samples from HIV-infected cases (n = 13) and HIV-uninfected controls (n = 13) from 2001-2015. Cases and controls were matched by histology and stage. Immunostained tumor sections were analyzed for percent of tumor cells expressing PD-L1 and B7-H3, and percent of tumor infiltrating immune cells (TII) expressing PD-1 and PD-L1. Positive expression was defined as >5%. Statistical analysis was performed using the non-parametric Mann-Whitney test and the chi-square test.

RESULTS

PD-L1 expression on tumor cells was positive in 23% of cases and 46% of controls. B7-H3 expression on tumor cells was positive in 92% of cases and 69% of controls. PD-1 expression on TII was positive in 69% of cases and 54% of controls. PD-L1 expression on TII was positive in 31% of cases and 69% of controls. B7-H3 percent expression on tumor cells was significantly higher in cases vs. controls (median 90% vs 20%, p = 0.005), but there were no significant differences in percent expression of PD-L1 on tumor cells, PD-1 on TII or PD-L1 on TII.

CONCLUSIONS

HIV-infected lung cancer patients had significantly higher B7-H3 tumor expression compared to HIV-uninfected controls, with similar rates of tumor PD-L1 expression, as well as PD-1 and PD-L1 expression on TII. These results support inclusion of HIV-infected lung cancer patients in future immunotherapy trials.

Osteosarcoma is an aggressive type of bone tumor that commonly occurs in pediatric age groups. The complete molecular mechanisms behind osteosarcoma formation and progression require elucidation. B7-H3 is a protein of the B7 family that acts as a co-stimulatory molecule with a significant role in adaptive immune responses. The link between B7-H3 expression and its role in different types of cancer remains unclear. B7-H3 protein exhibits different functional roles in in vivo and in vitro conditions that remain controversial. In the present study, a murine model of osteosarcoma was successfully established using a modified protocol so as to easily obtain a low grade and metastatic form of osteosarcoma tissue without complication. Histological data showed that a less organized and highly proliferative mass of cells was observed in the osteosarcoma tissue. A higher expression level of B7-H3 protein was also observed at each advanced stage of osteosarcoma, which indicated the contributory role of the protein in the development of the primary and metastatic forms of osteosarcoma. Immunohistochemistry was performed, which showed that the overexpression of B7-H3 protein in the metastatic form of osteosarcoma may be associated with its migration and invasion.

Objective To generate mouse anti-human monoclonal antibodies against the molecules expressed on immune cells from malignant pleural effusions, and identify the antigen recognized by the monoclonal antibody named Y4F11. Methods The cells separated from pleural effusions of lung cancer patients were used to immunize BALB/c mice. Hybridoma technology was used for cell fusion and screening; the monoclonal antibody named Y4F11 was chosen as the object for the following experiment. Flow cytometry was performed to analyze the molecules expressed on naive and activated T, B, NK cells and monocytes; Co-immunoprecipitation was conducted to get the antigen pulled down by Y4F11. Mass spectrometry sequencing and BLASTP were used to identify the antigen molecules. Western blotting, dot-blotting and flow cytometry were utilized to identify Y4F11. Results The study obtained 78 hybridoma clones secreting antibodies stably which could recognize surface molecules on cells from pleural effusions. The hybridoma named Y4F11 was chosen as the following experiment object for further identification. The molecule which Y4F11 recognized was about 50 Kd, and further was confirmed as B7-H3 molecule. Furthermore, Y4F11 could recognize B7-H3 expressed on B7-H3 gene-transferred cells as well as B7-H3 fusion protein. Besides, the expression pattern of B7-H3 on immune cells was confirmed by Y4F11 antibody. All these results indicated that the antigen molecule recognized by Y4F11 antibody was B7-H3. Conclusion A hybridoma cell line with stable expression of monoclonal antibody B7-H3 has been successfully obtained and could be used for biological function study on B7-H3.

The aim of this study was to analyze the expressions and significance of B7-H3 and CTLA-4 in the clinical stages of non-small-cell lung cancer (NSCLC). Seventy patients with NSCLC who underwent surgical resection or biopsy between January 2016 and February 2018 were enrolled. Among them, 30 were cases of paracancerous tissues and were assigned to the control group (CON). These cases were analyzed using immunochemical methods. Of the 70 cases, 48 were of adenocarcinoma, 19 were of squamous cell carcinoma, and 3 were of adenosquamous carcinoma. The expression rates of B7-H3 and CTLA-4 in the observation group (OBS) were 64.2% and 57.1% respectively, and those in the CON group were 6.7% and 0%, respectively (χ²=27.988, 28.571, P<0.001). The expression levels of B7-H3 and CTLA-4 in patients with poor differentiation, in stages III-IV, or with lymph node metastasis were significantly higher than those in patients with good-to-moderate differentiation, in stages I-II, and without lymph node metastasis (P<0.05). There was a positive correlation between the expressions of B7-H3 and CTLA-4 in the OBS group (r=0.74, P<0.05). B7-H3 and CTLA-4 are highly expressed and positively correlated with each other in NSCLC patients and are also closely related to clinical stages.

Objective: Pediatric diffuse gliomas (pDGs) are relatively rare and molecularly distinct from pediatric pilocytic astrocytoma and adult DGs. Immunotherapy is a promising therapeutic strategy, requiring a deep understanding of tumor immune profiles. The spatial locations of brain tumors might be related to the molecular profiles. We aimed to analyze the relationship between the immune checkpoint molecules with the locations of DGs comparing pediatric with adult patients. Method: We studied 20 pDGs patients (age ≤ 21 years old), and 20 paired adult patients according to gender and histological types selected from 641 adult patients with DGs. Immune checkpoint molecules including B7-H3, CD47, and PD-L1, as well as tumor-infiltrating lymphocytes (TILs) and tumor-associated macrophages (TAMs), were manifested by immunohistochemical staining. Expression difference analyses and Spearman's correlation were performed. MRI data were voxel-wise normalized, segmented, and analyzed by Fisher's exact test to construct the tumor frequency and p value heatmaps. Survival analyses were conducted by Log-rank tests. Result: The median age of pediatric patients was 16 years. 55% and 30% of patients were WHO II and III grades, respectively. The left frontal lobe and right cerebellum were the statistically significant locations for pDGs, while the anterior horn of ventricles for adult DGs. A potential association between the expression of PD-L1 and TAMs was found in pDGs (p = 0.002, R = 0.670). The right posterior external capsule and the lateral side of the anterior horn of the left ventricle were predominant locations for the adult patients with high expression of B7-H3 and low expression of PD-L1 compared to pediatric ones, respectively. Pediatric patients showed significantly improved overall survival compared with adults. The prognostic roles of immune checkpoint molecules and TILs/TAMs were not significantly different between the two groups. Conclusion: Immune checkpoint-associated locations of diffuse gliomas comparing pediatric with adult patients could be helpful for the immunotherapy decisions and design of clinical trials.

Keywords: B7-H3; CD47; PD-L1; immune checkpoint molecules; immunotherapy; pediatric diffuse gliomas; spatial locations.

OBJECTIVE

To investigate the effect and mechanism of targeted B7-H3 gene silencing on the tumorigenesis and metastasis of human hematological malignancy xenograft tumor in nude mice.

METHODS

Real-time fluorogentic quantitative PCR (qPCR) and flow cytometry (FCM) were used to detect the expression of B7-H3 in 13 strains of malignant hematologic cells. Then, U937, Maver and Z138 cells which expressed high level of B7-H3 were screened out. Targeted B7-H3 knockdown in U937, Maver and Z138 was performed by lentivirus transduction and the effect of B7-H3 silencing in stable cell lines was tested by qPCR and FCM. Injecting the nine groups subcutaneously into the nude mice to establish xenograft models after dividing the U937, Maver and Z138 into non-infected control group (CON), B7-H3 knockdown group (KD) and negative non-targeted control infected group (NC),respectively, for detecting the tumorigenicity and metastasis in vivo. Furthermore, the expression of Ki-67 in xenograft tumors was detected by immunohistochemistry (IHC). The expression of metalloproteinase 2 (MMP-2) was detected by western blot.

RESULTS

The stable B7-H3 silencing cell lines of U937, Maver and Z138 were successfully established. Compared with the NC group, the KD groups of U937, Maver and Z138 had an obviously slower tumor growth. The average tumor inhibition rates at the end of observation period were 61.83% (F=43.78, P<0.05), 59.12% (F=36.51, P<0.05) and 67.37% (F=40.29, P<0.05); there was no significant difference in tumor volume growth between the NC group and the CON group (P>0.05). The liver distant metastasis of all the xenograft tumor models in nude mice was the most common and the rates of distant metastasis in KD groups were significantly lower than that of the corresponding NC groups. The Ki-67 indexes of the KD groups were significantly lower than those of the relative NC groups in three cell lines (U937: 40.3%±5.2% vs. 79.1%±6.3%, q=30.31, P<0.05, Maver: 35.2%±6.4% vs. 69.6%±5.1%, q=24.82, P<0.05; Z138: 38.4%±7.1% vs. 75.7%±4.8%, q=28.07, P<0.05); there was no significant difference in the expression of Ki-67 between the NC group and the CON group (P>0.05). The expressions of MMP-2 were also significantly lower in the KD groups than in the NC groups (U937: q=14.59, P<0.05; Maver: q=9.25, P<0.05; Z138: q=11.04, P<0.05); there was no significant difference in the expression of MMP-2 between the NC group and the CON group (P>0.05).

CONCLUSIONS

Targeted B7-H3 gene silencing could inhibit the tumorigenesis and metastasis of human hematological malignancy xenograft tumor in nude mice. The mechanism may be related to the down-regulation of Ki-67 and MMP-2.

This study aimed to investigate molecule B7-H3 expression profiles of patients with ankylosing spondylitis (AS) and the clinical significance of B7-H3 in the pathogenesis of AS. Serum B7-H3 levels were measured by ELISA in patients with AS and healthy controls. The expression of B7-H3 protein and mRNA on CD14+ monocytes of peripheral blood mononuclear cells (PBMCs) and serum levels of T cell-associated cytokines were also analyzed. The serum B7-H3 levels in AS patients were significantly lower than in healthy controls. The expression of B7-H3 protein and mRNA on CD14+ monocytes of PBMCs and serum levels of TNF-α, IL-6, and IL-17A in AS patients were significantly higher than in controls. The reduced serum B7-H3 level was highly negatively correlated with AS Disease Activity Score (ASDAS), TNF-α, and IL-17A. Upregulated B7-H3 protein may play a role in the pathogenesis of AS by binding its receptor on T cells.

[This corrects the article on p. 1253 in vol. 6, PMID: 24179504.].

Cytochrome P450 1B1 (CYP1B1) is a phase I xenobiotic-metabolizing enzyme (XME) that is overexpressed in colorectal cancer (CRC) tissue, but the prognosis value of CYP1B1 in CRC remains elusive. Additionally, B7-H3 has a key role in tumor cell immune evasion by inhibiting functions of T cells. Thus, in this study, we aimed to identify a new marker for predicting the prognosis of CRC and to study the relationship between tumor metabolism and tumor immunity. We analyzed CYP1B1 and B7-H3 expression in 231 patients with CRC using immunohistochemistry, and we investigated the relationship between CYP1B1 and B7-H3 expression using real-time PCR and Western blot analysis in two human CRC cell lines. Kaplan-Meier survival analysis was used to calculate overall survival (OS) rates, and Cox proportional regression model was performed for multivariate analysis. We found that both CYP1B1 and B7-H3 expression were aberrantly increased in CRC tissues compared to normal colorectal tissues. Moreover, high expression of CYP1B1 was significantly correlated with poor OS, and multivariate analysis indicated that CYP1B1 was a valuable independent prognostic biomarker. Furthermore, CYP1B1 expression was significantly correlated with B7-H3 expression in CRC tissues samples and two human CRC cell lines. In conclusion, these results indicate that CYP1B1 may be a novel predictive biomarker for prognosis of CRC patients, and there is a strong correlation between CYP1B1 and B7-H3 in vivo and in vitro.

Ductal carcinoma in situ (DCIS) will account for 62,930 cases of breast cancer in 2019. DCIS is a pre-invasive lesion which may not progress to invasive carcinoma, yet surgery remains the mainstay treatment. Molecular imaging of a specific marker for DCIS grade for detection and active surveillance are critically needed to reduce potential overtreatment. First, breast cancer marker B7-H3 (CD276) expression was evaluated by immunohistochemical staining in 123 human specimens including benign epithelium (H-score 10.0 ± 8.2) and low (20.8 ± 17.7), intermediate (87.1 ± 69.5), and high (159.1 ± 87.6) grade DCIS, showing a positive association with DCIS nuclear grade (P < 0.001, AUC 0.96). Next, a murine DCIS model was combined with ultrasound molecular imaging of B7-H3 targeted microbubbles to differentiate normal glands from those harboring DCIS (n = 100, FVB/N-Tg(MMTVPyMT)634Mul, AUC 0.89). Finally, photoacoustic and fluorescence molecular imaging with an anti-B7-H3 antibody-indocyanine green conjugate were utilized for DCIS detection (n = 53). Molecular imaging of B7-H3 expression may allow for active surveillance of DCIS.

Objective: The proportion of patients with stage I lung adenocarcinoma (LUAD) has dramatically increased with the prevalence of low-dose computed tomography use for screening. Up to 30% of patients with stage I LUAD experience recurrence within 5 years after curative surgery. A robust risk stratification tool is urgently needed to identify patients who might benefit from adjuvant treatment.

Methods: In this first investigation of the relationship between metabolic reprogramming and recurrence in stage I LUAD, we developed a recurrence-associated metabolic signature (RAMS). This RAMS was based on metabolism-associated genes to predict cancer relapse and overall prognoses of patients with stage I LUAD. The clinical significance and immune landscapes of the signature were comprehensively analyzed.

Results: Based on a gene expression profile from the GSE31210 database, functional enrichment analysis revealed a significant difference in metabolic reprogramming that distinguished patients with stage I LUAD with relapse from those without relapse. We then identified a metabolic signature (i.e., RAMS) represented by 2 genes (ACADM and RPS8) significantly related to recurrence-free survival and overall survival times of patients with stage I LUAD using transcriptome data analysis of a training set. The training set was well validated in a test set. The discriminatory power of the 2 gene metabolic signature was further validated using protein values in an additional independent cohort. The results indicated a clear association between a high risk score and a very poor patient prognosis. Stratification analysis and multivariate Cox regression analysis showed that the RAMS was an independent prognostic factor. We also found that the risk score was positively correlated with inflammatory response, the antigen-presenting process, and the expression levels of many immunosuppressive checkpoint molecules (e.g., PD-L1, PD-L2, B7-H3, galectin-9, and FGL-1). These results suggested that high risk patients had immune response suppression. Further analysis revealed that anti-PD-1/PD-L1 immunotherapy did not have significant benefits for high risk patients. However, the patients could respond better to chemotherapy.

Conclusions: This study is the first to highlight the relationship between metabolic reprogramming and recurrence in stage I LUAD, and is the first to also develop a clinically feasible signature. This signature may be a powerful prognostic tool and help further optimize the cancer therapy paradigm.

Keywords: Lung adenocarcinoma; immune landscape; metabolic signature; recurrence; stage I.

T cells play a vital role in the immune responses against tumors. Costimulatory or coinhibitory molecules regulate T cell activation. Immune checkpoint inhibitors, such as programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1) have shown remarkable benefits in patients with various tumor, but few patients have displayed significant immune responses against tumors after PD-1/PD-L1 immunotherapy and many have been completely unresponsive. Thus, researchers must explore novel immune checkpoints that trigger durable antitumor responses and improve clinical outcomes. In this regard, other B7 family checkpoint molecules have been identified, namely PD-L2, B7-H2, B7-H3, B7-H4 and B7-H6. The aim of the present article was to address the expression, clinical significance and roles of B7 family molecules in lymphoma, as well as in T and NK cell-mediated tumor immunity. B7 family checkpoints may offer novel and immunotherapeutic strategies for patients with lymphoma.

Keywords: B7-H2; B7-H3; B7-H4; B7-H6; PD-L1; PD-L2; lymphoma.

Objective: B7-H3 is a member of the B7 family of immune checkpoint molecule. Although B7-H3 has been shown to regulate T cell-mediated peripheral immune response, whether it also correlated with NK cell exhaustion in ovarian cancer remains unclear. The purpose of this study was to explore the mechanism of B7-H3 regulating NK-cell proliferation and function.

Material and methods: To investigate the relationship between B7-H3 expression and the NK-cell function in ovarian cancer, human ovarian tumor tissues and cell lines were first examined the protein and mRNA expression of B7-H3 by quantitative real-time PCR (qRT-PCR), Immunohistochemistry and Western-blot assays. Then we established B7-H3 knockout cell lines and measured the cytotoxicity of NK cells on these cells by LDH release assay and Flow Cytometry. In addition, we analyzed B7-H3 in the regulation of glycolysis and glycolysis-related proteins by Glycolysis Stress Test, Glucose Consumption Assay and Western-blot. Moreover, luciferase reporter assay was used to confirm the directly regulation of miR-29c to B7-H3. Finally, we carried out in vivo experiments.

Results: We observed that tumor-expressed B7-H3 inhibits NK-cell function in vitro and in vivo, and is associated with glycolysis of ovarian cancer cell. Therapeutically, B7-H3 blockade prolonged the survival of SKOV3 tumor-bearing mice. In addition, miR-29c improved the anti-tumor efficacy of NK-cell by directly targeting B7-H3 in vitro were observed, but not in vivo.

Conclusion: Our results demonstrate that miR-29c downregulates B7-H3 to inhibit NK-cell exhaustion and associated with glycolysis, which suggest that NK cells may be a new target of anti-B7-H3 therapy in ovarian cancer patients.

Keywords: B7-H3; NK cells; Ovarian cancer; miR-29c.

Craniopharyngiomas (CPs) are uncommon intracranial benign neoplasms that located in sellar/parasellar region with clinically challenging. B7-H3 is an immune checkpoint molecule highly expressed in many malignant tumors. In this study, we analyzed whether B7-H3 is expressed in 44 CPs samples (adamantinomatous CPs: n = 30 and papillary CPs: n = 14), and whether it could serve as an immunotherapy target in CPs. Immunohistochemical analysis showed that B7-H3 was highly expressed in adamantinomatous CPs (184.3 ± 13.58) and papillary CPs (223.2 ± 11.89), while almost undetectable in normal brain tissue (24 ± 4.9). Besides, B7-H3 expression level was correlated with poor prognosis of patients with CPs. Immunofluorescence and Western blot analysis further suggested that β-catenin co-localized with B7-H3 and could promote its expression in adaCPs. B7-H3 expression level was positively correlated with staining intensity of IBA1⁺ cells, but negatively with T cell infiltration in CPs, suggesting that B7-H3 might play a role in the regulation of tumor microenvironment in CPs. Moreover, B7-H3/CD3 bi-specific T cell engager (BiTE) efficiently inhibited the growth of human primary craniopharyngioma cells in a time- and dose-dependent manner. Our results revealed B7-H3 was highly expressed in CPs and targeting B7-H3 might therefore be an effective therapeutic strategy against craniopharyngioma.

OBJECTIVE

To detect the serum levels of soluble B7-H3 (sB7-H3) and interferon γ (IFN-γ) in patients with hepatitis B and related clinical implications.

METHODS

The levels of sB7-H3 and IFN-γ were detected by ELISA in 87 cases of hepatitis B including 16 cases of acute hepatitis, 25 cases of chronic moderate to severe hepatitis, 24 cases of liver cirrhosis, 22 cases of decompensated cirrhosis, and 24 healthy subjects. Their correlations with the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), α-fetoprotein (AFP), white blood cells (WBCs), hepatitis virus B (HBV) DNA were analyzed statistically.

RESULTS

The serum levels of sB7-H3 and IFN-γ in patients with hepatitis B were (202.17 ± 58.14) ng/mL and (3436.11 ± 1605.01) pg/mL, respectively, which were significantly higher than those in the healthy subjects. SB7-H3 was closely related to IFN-γ. AST, ALT, AFP, WBCs, and HBV DNA had no correlations with sB7-H3 and IFN-γ. SB7-H3 was the highest in the patients with acute hepatitis, while IFN-γ was the highest in the patients with chronic hepatitis B.

CONCLUSIONS

The levels of sB7-H3 and IFN-γ in the patients with hepatitis B are higher than those in the healthy subjects. Continuous monitoring of serum sB7-H3 and IFN-γ may helpful in predicting disease outcomes for patients with hepatitis B.