Augmentation of cellular immune response by Ipomoea obscura and Ipobscurine alkaloid attenuates tumor growth in mice

2011 ◽  
Vol 89 (4) ◽  
pp. 259-268 ◽  
Author(s):  
T.P. Hamsa ◽  
Girija Kuttan
Keyword(s):  
Immune Response ◽  
Tumor Growth ◽  
Immune Status ◽  
Interleukin 2 ◽  
Cell Activity ◽  
Indole Alkaloid ◽  
Tumor Bearing ◽  
Cell Mediated Immune Response ◽  
Ifn Γ ◽  
Ipomoea Obscura

The immune status of the host plays a crucial role in controling the process of carcinogenesis. General or selective activation of various immunocompetent cells and their secretory function to maintain a healthy immune status may help in cancer prophylaxis, as well as therapy. The present study focused on the effect of Ipomoea obscura and Ipobscurine on cell-mediated immune response. In this study we evaluated the effect of I. obscura and an indole alkaloid fraction from I. obscura on effector mechanisms of cell-mediated immune response by analyzing cytotoxic T lymphocyte (CTL) activity, natural killer (NK) cell activity, antibody-dependent cell-mediated cytotoxicity (ADCC), and antibody-dependent complement-mediated cytotoxicity (ACC). The effect of I. obscura and Ipobscurine on interleukin-2 (IL-2) and interferon-γ (IFN-γ) levels was also analyzed. In the in vitro and in vivo systems, I. obscura and Ipobscurine treatment augmented cell-mediated immune response by enhancing the killing activity of CTL and NK cells from splenocytes in normal as well as tumor-bearing mice. ADCC and ACC were also enhanced significantly in both normal and tumor-bearing animals after drug administration, compared with untreated control. Administration of I. obscura and Ipobscurine significantly enhanced the production of IL-2 and IFN-γ in normal as well as tumor-bearing animals. This study reveals that both I. obscura and Ipobscurine have the potential to augment immune response through the enhanced secretion of IL-2 and IFN-γ by T cells and thereby inhibit tumor growth and as an alternative medicine for cancer treatment.

scholarly journals Checkpoint blockade accelerates a novel switch from an NKT-driven TNFα response toward a T cell driven IFN-γ response within the tumor microenvironment

2021 ◽  
Vol 9 (6) ◽  
pp. e002269
Author(s):  
Shota Aoyama ◽  
Ryosuke Nakagawa ◽  
Satoshi Nemoto ◽  
Patricio Perez-Villarroel ◽  
James J Mulé ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
T Cell ◽  
Tumor Growth ◽  
Ex Vivo ◽  
T Cell Response ◽  
Effector Function ◽  
Checkpoint Blockade ◽  
Necrosis Factor Alpha ◽  
Ifn Γ

BackgroundThe temporal response to checkpoint blockade (CB) is incompletely understood. Here, we profiled the tumor infiltrating lymphocyte (TIL) landscape in response to combination checkpoint blockade at two distinct timepoints of solid tumor growth.MethodsC57BL/6 mice bearing subcutaneous MC38 tumors were treated with anti-PD-1 and/or anti-CTLA-4 antibodies. At 11 or 21 days, TIL phenotype and effector function were analyzed in excised tumor digests using high parameter flow cytometry. The contributions of major TIL populations toward overall response were then assessed using ex vivo cytotoxicity and in vivo tumor growth assays.ResultsThe distribution and effector function among 37 distinct TIL populations shifted dramatically between early and late MC38 growth. At 11 days, the immune response was dominated by Tumor necrosis factor alpha (TNFα)-producing NKT, representing over half of all TIL. These were accompanied by modest frequencies of natural killer (NK), CD4+, or CD8+ T cells, producing low levels of IFN-γ. At 21 days, NKT populations were reduced to a combined 20% of TIL, giving way to increased NK, CD4+, and CD8+ T cells, with increased IFN-γ production. Treatment with CB accelerated this switch. At day 11, CB reduced NKT to less than 20% of all TIL, downregulated TNFα across NKT and CD4+ T cell populations, increased CD4+ and CD8+ TIL frequencies, and significantly upregulated IFN-γ production. Degranulation was largely associated with NK and NKT TIL. Blockade of H-2kb and/or CD1d during ex vivo cytotoxicity assays revealed NKT has limited direct cytotoxicity against parent MC38. However, forced CD1d overexpression in MC38 cells significantly diminished tumor growth, suggesting NKT TIL exerts indirect control over MC38 growth.ConclusionsDespite an indirect benefit of early NKT activity, CB accelerates a switch from TNFα, NKT-driven immune response toward an IFN-γ driven CD4+/CD8+ T cell response in MC38 tumors. These results uncover a novel NKT/T cell switch that may be a key feature of CB response in CD1d+ tumors.

scholarly journals Polarization of Allogeneic T-Cell Responses by Influenza Virus-Infected Dendritic Cells

2000 ◽  
Vol 74 (17) ◽  
pp. 7738-7744 ◽  
Author(s):  
Sangkon Oh ◽  
Maryna C. Eichelberger
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Dendritic Cells ◽  
Influenza Virus ◽  
T Cell ◽  
Interleukin 2 ◽  
Dependent Manner ◽  
Ifn Γ ◽  
High Doses ◽  
Type Response

ABSTRACT The developing immune response in the lymph nodes of mice infected with influenza virus has both Th1- and Th2-type characteristics. Modulation of the interactions between antigen-presenting cells and T cells is one mechanism that may alter the quality of the immune response. We have previously shown that the ability of dendritic cells (DC) to stimulate the proliferation of alloreactive T cells is changed by influenza virus due to viral neuraminidase (NA) activity. Here we show that DC infected with influenza virus A/PR/8/34 (PR8) stimulate T cells to produce different types of cytokines in a dose-dependent manner. Optimal amounts of the Th1-type cytokines interleukin-2 (IL-2) and gamma interferon (IFN-γ) were produced from T cells stimulated by DC infected with low doses of PR8, while the Th2-type cytokines IL-4 and IL-10 were produced only in response to DC infected with high doses of PR8. IL-2 and IFN-γ levels corresponded with T-cell proliferation and were dependent on the activity of viral NA on the DC surface. In contrast, IL-4 secretion required the treatment of T cells with NA. Since viral particles were released only from DC that are infected with high doses of PR8, our results suggest that viral NA on newly formed virus particles desialylates T-cell surface molecules to facilitate a Th2-type response. These results suggest that the activity of NA may contribute to the mixed Th-type response observed during influenza virus infection.

scholarly journals Predominance of Th1 Immune Response in Pleural Effusion of Patients with Tuberculosis among Other Exudative Etiologies

2019 ◽  
Vol 58 (1) ◽  
Author(s):  
Vinícius da Cunha Lisboa ◽  
Marcelo Ribeiro-Alves ◽  
Raquel da Silva Corrêa ◽  
Isabelle Ramos Lopes ◽  
Thiago Thomaz Mafort ◽  
...  
Keyword(s):  
Immune Response ◽  
Pleural Effusion ◽  
Transforming Growth Factor ◽  
Interleukin 2 ◽  
Principal Component ◽  
Transforming Growth Factor Β1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Biochemical Tests ◽  
Cross Sectional ◽  
Ifn Γ

ABSTRACT Pleural tuberculosis (PlTB), a common form of extrapulmonary TB, remains a challenge in the diagnosis among many causes of pleural effusion. We recently reported that the combinatorial analysis of interferon gamma (IFN-γ), IFN-γ-inducible protein 10 (IP-10), and adenosine deaminase (ADA) from the pleural microenvironment was useful to distinguish pleural effusion caused by TB (microbiologically confirmed or not) among other etiologies. In this cross-sectional cohort study, a set of inflammatory mediators was quantified in blood and pleural fluid (PF) from exudative pleural effusion cases, including PlTB (n = 27) and non-PlTB (nTB) (n = 25) patients. The levels of interleukin-2 (IL-2), IL-4, IL-6, IL-10, IL-17A, IFN-γ, tumor necrosis factor (TNF), IP-10, transforming growth factor β1 (TGF-β), and ADA were determined using cytometric bead assay, enzyme-linked immunosorbent assay (ELISA), or biochemical tests. IFN-γ, IP-10, TNF, TGF-β, and ADA quantified in PF showed significantly higher concentrations in PlTB patients than in nTB patients. When blood and PF were compared, significantly higher concentrations of IL-6 and IL-10 in PF were identified in both groups. TGF-β, solely, showed significantly increased levels in PF and blood from PlTB patients when both clinical specimens were compared to those from nTB patients. Principal-component analysis (PCA) revealed a T helper type 1 (Th1) pattern attributed mainly to higher levels of IP-10, IFN-γ, TGF-β, and TNF in the pleural cavity, which was distinct between PlTB and nTB. In conclusion, our findings showed a predominantly cellular immune response in PF from TB cases, rather than other causes of exudative effusion commonly considered in the differential diagnosis of PlTB.

scholarly journals Amelioration of B16F10 melanoma lung metastasis in mice by a combination therapy with indomethacin and interleukin 2.

1987 ◽  
Vol 165 (1) ◽  
pp. 14-28 ◽  
Author(s):  
R S Parhar ◽  
P K Lala
Keyword(s):  
Combination Therapy ◽  
Lung Metastasis ◽  
Lung Metastases ◽  
Killer Cell ◽  
Interleukin 2 ◽  
Cell Activity ◽  
Cell Phenotype ◽  
B16f10 Melanoma ◽  
Killer Activity ◽  
Tumor Bearing

Our earlier work revealed that PGE-mediated inactivation of NK cells in tumor-bearing mice by host macrophages promoted spontaneous lung metastasis that could be prevented or ameliorated by chronic indomethacin therapy. Since PGE was found to suppress the in vitro development and/or activation of a family of tumoricidal lymphocytes such as CTL, NK, and LAK cells by one or both of two mechanisms, that is to say, a down regulation of IL-2-R and an inhibition of IL-2 production, the present study tested whether a combined therapy with indomethacin and IL-2 was more effective than one with indomethacin or IL-2 alone in ameliorating established experimental lung metastasis. B6 mice injected intravenously with 10(6) highly metastatic B16F10 melanoma cells showed profuse micrometastases in the lungs by day 5, and macrometastases by day 10 which were confluent on day 21. Chronic indomethacin therapy by the oral route (14 micrograms/ml in drinking water) starting on day 0 or day 5, or a single round of IL-2 therapy (25,000 U rIL-2, every 8 h for 5 d on days 10-14) reduced the number of metastatic nodules by two-thirds (from a median of 473 in control mice receiving vehicles alone) by day 21. A single round of IL-2 as above, combined with either protocol of indomethacin therapy, completely or nearly completely irradicated the lung metastases, corroborated by a histological examination. An evaluation of splenic killer cell activity measured with a 4-h 51Cr-release assay against NK-sensitive YAC-1 lymphoma and B16F10 melanoma or NK-resistant thymic lymphoma 9705 targets revealed negligible activity in control tumor-bearing mice, and a good restoration of activity against NK-sensitive targets with either protocols of indomethacin therapy. IL-2 alone or a combination of IL-2 and indomethacin given by either protocol generated strong killer activity against all these targets, most marked with the combination therapy. Splenic killer cell phenotype in normal as well as all treated animals was ASGM1+, Thy-1-, and Lyt-2-. The combination therapy resulted in the strongest mononuclear cell infiltration in the lungs, with areas of young granulation tissue suggestive of repair sites of original metastases.

scholarly journals Control of Heterologous Hepatitis C Virus Infection in Chimpanzees Is Associated with the Quality of Vaccine-Induced Peripheral T-Helper Immune Response

2004 ◽  
Vol 78 (1) ◽  
pp. 187-196 ◽  
Author(s):  
C. Rollier ◽  
E. Depla ◽  
J. A. R. Drexhage ◽  
E. J. Verschoor ◽  
B. E. Verstrepen ◽  
...  
Keyword(s):  
Immune Response ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Interleukin 2 ◽  
Hcv Infection ◽  
T Helper ◽  
Vaccine Strategy ◽  
Ns3 Protein ◽  
Ifn Γ

ABSTRACT Prophylactic hepatitis C virus (HCV) vaccine trials with human volunteers are pending. There is an important need for immunological end points which correlate with vaccine efficacy and which do not involve invasive procedures, such as liver biopsies. By using a multicomponent DNA priming-protein boosting vaccine strategy, naïve chimpanzees were immunized against HCV structural proteins (core, E1, and E2) as well as a nonstructural (NS3) protein. Following immunization, exposure to the heterologous HCV 1b J4 subtype resulted in a peak of plasma viremia which was lower in both immunized animals. Compared to the naïve infection control and nine additional historical controls which became chronic, vaccinee 2 (Vac2) rapidly resolved the infection, while the other (Vac1) clearly controlled HCV infection. Immunization induced antibodies, peptide-specific gamma interferon (IFN-γ), protein-specific lymphoproliferative responses, IFN-γ, interleukin-2 (IL-2), and IL-4 T-helper responses in both vaccinees. However, the specificities were markedly different: Vac2 developed responses which were lower in magnitude than those of Vac1 but which were biased towards Th1-type cytokine responses for E1 and NS3. This proof-of-principle study in chimpanzees revealed that immunization with a combination of nonstructural and structural antigens elicited T-cell responses associated with an alteration of the course of infection. Our findings provide data to support the concept that the quality of the response to conserved epitopes and the specific nature of the peripheral T-helper immune response are likely pivotal factors influencing the control and clearance of HCV infection.

scholarly journals PROTEIN REKOMBINAN 38 KDA MYCOBAKTERIUM TUBERKULOSIS DAPAT MENGIMBAS PEMBUATAN INTERLEUKIN-2 DAN INTERFERON-γ LIMFOSIT T DI KULTUR SEL MONONUKLEAR DARAH TEPI

2018 ◽  
Vol 22 (2) ◽  
pp. 151
Author(s):  
Maimun Z Arthamin ◽  
Singgih Pujo Wahono ◽  
Antiek Primardianti ◽  
Ati Rastini ◽  
Tri Wahju Astuti ◽  
...  
Keyword(s):  
Immune Response ◽  
T Lymphocytes ◽  
Recombinant Protein ◽  
Vaccine Development ◽  
Interleukin 2 ◽  
Development Program ◽  
In Vitro Study ◽  
Cell Mediated Immunity ◽  
Ifn Γ

Tuberculosis (TB) is caused by Mycobacterium tuberculosis (M.tb) and is one of the significant mortality causes WHO (2012). Theprimary immune response in TB pathogenesis is Cell Mediated Immunity (CMI), roled by T lymphocytes. Interleukin-2 (IL-2) is a growthfactor for T lymphocytes. Gamma Interferon is the key cytokine in M.tb infection control, synthezised by T lymphocytes. An effectivevaccination strategy is achieved by giving vaccine which is able to stimulate T lymphocytes in synthezising cytokines. The 38 kDa M.tbprotein is potential in the vaccine development program, because it has specific epitopes for T lymphocytes. The aim of this study was toknow how to determine that the 38 kDa recombinant protein of M.tb Malang strain could induce cellular immune response by IL-2 andIFN-γ synthezised by T lymphocytes. The study was carried out by an experimental in vitro study on PBMC from healthy endemic subjects,those having TB contact, and the TB patients themselves. PBMC from subjects was cultured with 38 kDa recombinant protein of M.tbMalang strain, with PPD and without any protein. The analysis of IL-2 and IFN-γ used flowcytometry. The result showed that the highestpercentage of IL-2 was found in the culture with 38 kDa recombinant protein of M.tb Malang strain, in healthy endemic (p=0.000)and in those who had TB contact (p=0.000). the highest percentage of IFN-γ was found in the culture with 38 kDa recombinant proteinof M.tb Malang strain, in healthy endemic (p=0.007) and those who had TB contact (p = 0.105). The 38 kDa recombinant proteinof M.tb Malang strain was able to induce IL-2 and IFN-γ synthezised by TCD3+ lymphocytes from healthy endemic subjects and thosewho had TB contact.

scholarly journals TRPV1 modulation of immune response in metastatic breast carcinoma: Enhanced inflammatory response may hinder therapeutic potentials of TRPV1 agonists

2021 ◽  
Author(s):  
Nuray Erin ◽  
Muhlis Akman ◽  
Seren Haksever
Keyword(s):  
Immune Response ◽  
Breast Carcinoma ◽  
Immune Cells ◽  
Metastatic Breast ◽  
Inverse Agonist ◽  
Transient Receptor Potential Vanilloid ◽  
Metastatic Breast Carcinoma ◽  
Tumor Bearing ◽  
Trpv1 Channels ◽  
Ifn Γ

Abstract Background and Purpose: The transient receptor potential vanilloid 1 (TRPV1) ion channels enhance cytotoxic immune response and may have therapeutic potential in cancer treatment. Hence, we here determined how activation of TRPV1 alters immune response of tumor-bearing mice.Experimental Approach: Three different metastatic subset of 4T1 breast carcinoma cells were used to induce tumors in Balb-c mice. Mix leukocyte cultures (MLCs) using spleens and draining lymph nodes were prepared and stimulated with various challenges. Effects of four different TRPV1 agonists, antagonist (AMG9810) and Gambogic Amide (GA), a TrkA agonist that sensitizes TRPV1, on secreted levels of cytokines were determined.Results: MLCs of tumor-bearing mice secreted markedly higher levels of IL-6 and lower levels of IFN-γ compared to control mice. We observed differential effects of TRPV1 agonists, antagonist and GA in control and mice bearing different subset of metastatic cells. TRPV1 and TrkA agonists increased IFN--γ and IL-17 secretion in control mice while they markedly increased IL-6 secretion and suppressed IFN--γ secretion in tumor-bearing mice. Unexpectedly, AMG9810 acted as an inverse agonist and did not antagonize the effects of TRPV1 agonists and GA did not sensitize TRPV1 channels. Conclusions: Our results demonstrate constitutive activity of TRPV1 in immune cells, suggesting cross activation. Excessive chronic activation of TRPV1 in immune cells in the presence of metastatic breast carcinoma may have detrimental effects. Unexpected findings further document that a drug can have multiple intrinsic activities and depending on surrounding factors can act on the same receptor as an agonist, antagonist or inverse agonist.

scholarly journals Evolution of the Primary Immune Response toHistoplasma capsulatum in Murine Lung

1998 ◽  
Vol 66 (4) ◽  
pp. 1473-1481 ◽  
Author(s):  
Judith A. Cain ◽  
George S. Deepe
Keyword(s):  
Immune Response ◽  
Nk Cells ◽  
Interleukin 2 ◽  
Primary Immune Response ◽  
Pcr Analysis ◽  
Cell Populations ◽  
Mrna Levels ◽  
Cytoplasmic Staining ◽  
Inflammatory Reactions ◽  
Ifn Γ

ABSTRACT Histoplasma capsulatum induces a cell-mediated immune response in the lungs and lymphoid organs of mammals. In this study, we analyzed the progression of the cytokine and inflammatory reactions in the lungs of mice infected intranasally with H. capsulatum. We measured cytokine mRNA levels and determined the inflammatory cell populations during the active phase of infection (<3 weeks). Transcription of genes encoding interleukin-2 (IL-2), IL-4, and IL-12 and gamma interferon (IFN-γ) was detectable as early as day 3 of infection, whereas a signal for IL-10 was never observed. Competitive PCR analysis demonstrated that enhanced expression of IL-12 mRNA was observed by day 3 and that expression of mRNA for IL-2 and IFN-γ progressively increased from day 5 to day 10. All levels declined by day 14. Analysis of the inflammatory response revealed an initial elevation in myeloid cells (Mac-1+) and natural killer (NK) cells followed by a rise in T cells, predominantly CD4+cells. Since IFN-γ is a key factor in host defense, we performed cytoplasmic staining to determine the cell populations that produced this cytokine. The hierarchy of synthesis was CD4+ > CD8+ > NK cells. Thus, H. capsulatum provokes an orderly modulation of the inflammatory and cytokine responses in murine lungs.

Phenotype and antitumor activity of ascitic fluid monocytes in patients with ovarian carcinoma

2003 ◽  
Vol 13 (4) ◽  
pp. 435-443 ◽  
Author(s):  
B. Melichar ◽  
C. A. Savary ◽  
R. Patenia ◽  
S. Templin ◽  
K. Melicharova ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Interleukin 2 ◽  
Cell Activity ◽  
Antigen Expression ◽  
Cytostatic Activity ◽  
Interleukin 12 ◽  
Necrosis Factor Alpha ◽  
Color Flow ◽  
Uptake Inhibition ◽  
Ifn Γ

Monocytes/macrophages (MO/MA) represent a major leukocyte population in the peritoneal cavity of patients with epithelial ovarian cancer (EOC). We examined the phenotypic characteristics and antitumor cell activity of ascitic MO in patients with EOC. MO/MA phenotype was compared with MO in peripheral blood by two- and three-color flow cytometry. Cytotoxic/cytostatic effects of different cytokines on cultured EOC cells were measured by initial labeling or uptake inhibition of [methyl-3H] thymidine. Malignant ascites had higher proportion of MO/MA with the CD14brightCD16+ phenotype than peripheral blood. Cell surface antigen expression of activation and differentiation in peripheral blood and ascites, including CD38, CD40, CD64, and CD86, was higher on CD14brightCD16− and CD14brightCD16+ than on CD14dimCD16− cells. HLA-DR expression was higher on ascitic MO/MA than peripheral blood MO. Significant cytotoxic/cytostatic activity was elicited by treating ascitic MO/MA with interferon-γ (IFN-γ) and interleukin-2 (IL-2), but not with interleukin-12, paclitaxel, granulocyte-monocyte colony-stimulating factor (GM-CSF), or tumor necrosis factor-alpha (TNF-α). Soluble CD40Lt did not enhance MO/MA cytotoxic activity, and inhibited IFN-γ or IL-2 induced cytoxicity. We conclude that MO/MA from ascites have elevated proportions of CD14brightCD16+ cells, showing phenotypic features of activation. IFN-γ induces the cytotoxic and cytostatic activity of MO/MA that is inhibited by CD40Lt.

A Uracil Auxotroph Toxoplasma gondii Exerting Immunomodulation to Inhibit Breast Cancer Growth and Metastasis

2021 ◽  
Author(s):  
Li-Qing Xu ◽  
Li-Jie Yao ◽  
Dan Jiang ◽  
Min Chen ◽  
Wen-Zhong Liao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Toxoplasma Gondii ◽  
Tumor Growth ◽  
Lung Metastasis ◽  
Tumor Bearing ◽  
Uracil Auxotroph ◽  
Ifn Γ

Abstract Background: Breast cancer is the most common cause of cancer-related death among women, and patients with triple-negative breast cancer (TNBC) have poor prognosis, so it is necessary to develop new effective therapies urgently. Recent studies have demonstrated that uracil auxotroph Toxoplasma gondii vaccine displays antitumor effects. Here, we examined the immunotherapy effects of an attenuated uracil auxotroph strain of T. gondii against 4T1 murine breast cancer.Methods: We constructed a uracil auxotroph strain, the orotidine 5′-monophosphate decarboxylase gene deleted strain of T. gondii (RH-Δompdc) with the CRISPR/Cas9 technology. Its virulence in vitro and in vivo was determined by parasite replication assay, plaque assay, the parasite burden detection in mice peritoneal fluids and the survival analysis of T. gondii infection mice. Its immune modulation ability was evaluated by cytokines detection. Its antitumor effect was evaluated after its in situ inoculation to 4T1 tumors in mouse model, the tumor volume was measured, the 4T1 lung metastasis was detected by H&E and Ki67 antibody staining, and the cytokines levels were measured by ELISA.Results: RH-Δompdc strain could proliferate normally with uracil supplement, however, it was unable to propagate without uracil and in vivo, which implicated that it is avirulent to the hosts. This mutant showed vaccine characteristics that it could induce intense immune responses both in vitro and in vivo by boosting the expression of inflammatory cytokines significantly. RH-Δompdc in situ inoculation to the 4T1 tumors in mice could inhibit the tumor growth, reduce the lung metastasis, promote the survival of the tumor-bearing mice, and also increase the secretion of Th1 cytokines IL-12 and IFN-γ both in serum and in the tumor microenvironment (TME). Conclusion: The uracil auxotroph RH-Δompdc inoculation to the 4T1 tumors stimulated the anti-infection and antitumor immunity in mice, resulted in the inhibition of tumor growth and metastasis, the promotion in survival of the tumor-bearing mice, and the increasing secretion of IL-12 and IFN-γ both in serum and in the TME. Our findings implied that the immunomodulation resulted by RH-Δompdc could be a potential antitumor strategy.

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