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Objective:To investigate whether IL-7-secreting oncolytic herpes simplex virus(HSV)could activate CD8+T cells and inhibit the growth of hepatocellular carcinoma.Methods:The expression of IL-7 was detected by Western blot.The in vitro cleavage of tumor cells by tumor oncolytic virus HSV and HSV-IL-7 were detected by crystal violet staining.The tumor inhibition ability of HSV-IL-7 and HSV were detected in subcutaneous transplanted tumor model.Levels of IL-7,IFN-γ and TNF-α in serum and tumor tissues were determined by ELISA.The infiltration of CD8+T cells in tumor tissues was detected by immunohistochemistry.Flow cytometry was used to detect Granzyme B secretion in CD8+T cells infiltrated by tumor.Results:Tumor cells infected with HSV-IL-7 expressed high level of IL-7.Both HSV and HSV-IL-7 can effectively lyse B16-F10,CT-26 and H22 tumor cell lines in a dose-dependent manner in vitro.HSV-IL-7 could significantly inhibit the growth of H22 hepatoma cells in vivo(P<0.01)and prolong the survival time of tumor-bearing mice(P<0.001).HSV-IL-7 could significantly increase the IL-7 content in tumor sites(P<0.000 1),and effectively increase the number of tumor infiltrating CD8+T cells(P<0.001).HSV-IL-7 significantly enhanced Granzyme B secretion of tumor-infiltrating CD8+T cells and IFN-γ and TNF-α in tumor tissues(P<0.000 1).Conclusion:HSV-IL-7 has well tumor inhibition activity in vivo and in vitro.It also can activate the anti-tumor activity of CD8+T cells in vivo by secreting IL-7,inhibit tumor growth and prolong the survival time of tumor-bearing mice.
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Abstract Objective: To investigate the expression level and significance of T cell immunoglobulin and mucin-domain containing molecules-3 (Tim-3) and interleukin-7 (IL-7) in CD4+ T lymphocytes in peripheral blood of patients with coronary heart disease (CHD). Methods: 75 patients with CHD treated at our hospital were selected and classified as mild group (25 cases), moderate group (25 cases) and severe group (25 cases), according to the severity of illness. Twenty-five healthy volunteers who underwent a physical examination at our hospital during the same period were selected as the control group. The expression level of Tim-3 in CD4+ T lymphocytes in peripheral blood of patients in four groups was detected by flow cytometry and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). The expression level of IL-7 in peripheral blood serum was measured by enzyme-linked immunosorbent assay (ELISA). Correlation analyses of Tim-3 and IL-7, Tim-3 and disease severity and IL-7 and disease severity were performed, respectively. Results: Flow cytometry and qRT-PCR demonstrated that the expression of Tim-3 in CD4+ T lymphocytes in peripheral blood of patients with CHD increased with the aggravation of the disease. ELISA showed that the tendency of IL-7 expression in peripheral blood serum was consistent with the expression of Tim-3, and the expression of Tim-3 had a positive correlation with IL-7. The expression levels of both Tim-3 and IL-7 were positively correlated with the Gensini score. Conclusion: The expression of Tim-3 and IL-7 in peripheral blood of patients with CHD was upregulated and increased with the aggravation of CHD.
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Objective:To investigate the expression of membrane-bound CD127 (mCD127) and soluble CD127 (sCD127) in patients with sepsis, and to assess the mechanism of IL-7 in regulating CD8 + T cell activity in these patients. Methods:A prospective cohort study was conducted on 47 patients with sepsis (sepsis group) and 18 healthy controls (control group). Serum samples and peripheral blood mononuclear cells (PBMCs) were isolated. CD8 + T cells were purified. IL-7 and sCD127 levels in serum were measured by enzyme-linked immunosorbent assay. Expression of mCD127 on CD8 + T cells was measured by flow cytometry. Total CD127 and sCD127 expression at mRNA level in CD8 + T cells was semi-quantified by real-time PCR. CD8 + T cells were stimulated with recombinant human IL-7, along with signal transducer and activator of transcription 5 (STAT5) inhibitor or phosphatidylinositol 3-kinase (PI3K) inhibitor. Changes in mCD127 expression on CD8 + T cells and the expression of total CD127 and sCD127 at mRNA level were then measured. The cytotoxicity of CD8 + T cells in response to IL-7 stimulation was assessed using a co-culture system with CD8 + T cells and MCF-7 cells. Student′s t test and LSD- t test were used for statistical analysis. Results:Serum IL-7 and sCD127 were lower in sepsis group than in control group [(101.82±12.58) pg/ml vs (111.07±11.10) pg/ml, P<0.01; (278.58±62.31) pg/ml vs (334.62±70.55) pg/ml, P<0.01]. Serum IL-7 was positively correlated with serum sCD127 in patients with sepsis ( r=0.46, P<0.01). The percentage of mCD127 + CD8 + T cells in CD8 + T cells and the mean fluorescence intensity of mCD127 in sepsis group were higher than those in control group ( P<0.05). The expression of sCD127 at mRNA level in CD8 + T cells was lower in sepsis group than in control group (1.34±0.33 vs 1.80±0.60, P<0.001). Stimulation with recombinant human IL-7 promoted sCD127 secretion and total CD127 and sCD127 expression at mRNA level in CD8 + T cells ( P<0.05). Inhibition of STAT5 suppressed the IL-7-induced sCD127 secretion and total CD127 and sCD127 expression at mRNA level ( P<0.05). However, inhibition of PI3K could not achieve those effects ( P>0.05). CD8 + T cells-induced target cell death was inhibited in sepsis group as compared with that in control group [(12.49±2.12)% vs (23.83±3.76)%, P<0.001]. Recombinant human IL-7 promoted the CD8 + T cell-induced target cell death ( P<0.05) and increased the secretion of cytokines and cytotoxic granule proteins ( P<0.05). Inhibition of STAT5 suppressed IL-7-mediated CD8 + T cell cytotoxicity ( P<0.05). However, inhibition of PI3K did not affect IL-7-mediated CD8 + T cell cytotoxicity ( P>0.05). Conclusions:IL-7 promoted sCD127 secretion and enhanced the in vitro cytotoxicity of CD8 + T cells in patients with sepsis through STAT5 signal pathway.
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Objective:To explore the possible correlation between serum detection of IL-7, IL-21, HBV-specific cytotoxic T lymphocytes (CTLs), HBV DNA, and the expression of CD127 on the T lymphocytes, and discuss the effect of IL-7 to cellular immune response in patients with chronic hepatitis B (CHB).Methods:Five hundred and sixty serum samples were collected from patients with CHB in Beijing Friendship Hospital from September 2017 to March 2020. The serum IL-7 and IL-21 were detected by enzyme-linked immunosorbent assay (ELISA), and HBV-specific CTLs and the expression of CD127 on the T lymphocytes were determined by flow cytometry. While HBV DNA were tested using quantitative real-time PCR (qRT-PCR). Subjects were divided into groups A, B, and C, according to the IL-7 levels (low: IL-7<20 pg/ml, medium: 20 pg/ml≤IL-7<30 pg/ml, and high: IL-7≥30 pg/ml).Results:The average concentration of serum IL-7 in patients with CHB was significantly lower than that of healthy controls ( P<0.01), and the difference among three groups was statistically significant ( P<0.01). Meanwhile, levels of IL-21, percentages of HBV-specific CTL, and the expression of CD127 on the CD8 + T lymphocytes showed an upward trend among groups, and there were significant differences among three groups ( P<0.01) with a positive correlation between each two variables ( P<0.01). However, HBV DNA showed a downward trend in group A, B and C, and the difference of the three groups were statistically significant ( P<0.01), which were negatively correlated with other variables ( P<0.01). Multiple linear regression analysis showed that HBV-specific CTL was an independent influencing factor for HBV DNA ( P<0.01), and IL-7, the expression of CD127 on the CD8 + T lymphocytes and IL-21 had an independent effect on HBV-specific CTL ( P<0.05). Conclusions:IL-7 could regulate HBV-specific immune response, and might be used as an effective cellular immune indicator to evaluate the cellular immune status of patients with chronic hepatitis B.
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@#[Abstract] Objective: : To explore the impact of γ-chain (γc) family cytokines (IL-2, IL-7, IL-15, IL-21) on T cell phenotypes in ex vivo culture to provide experimental evidence for ex vivo cell preparation in adoptive immunotherapy. Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from peripheral blood of healthy volunteers; nylon column sorting, CD3+ magnetic beads sorting, CD3- magnetic beads sorting and natural sedimentation were used to sort T cells from PBMCs. The purity, recovery rate and viability of T cells sorted by the above methods were compared. The CD3/CD28 magnetic beads-activated CD3+T cells were cultured inAIMV medium with IL-2 or mixed cytokines (IL-7, IL-15, IL-21). The expansion fold and phenotypes of T cells in ex vivo culture were detected by flow cytometry. Results: : The purity of T cells sorted by CD3- magnetic beads sorting was significantly higher than that sorted by nylon column, CD3+ magnetic beads sorting and natural sedimentation ([94.06±1.07]% vs [86.74±1.06]%, [89.61±1.40]%, [88.48 ± 1.86]%, P<0.05); The recovery rate of T cells sorted by natural sedimentation was significantly higher than that by other three methods ([60.29±1.53]% vs [45.03±2.79]%, [20.15±3.41]%, [42.98±2.82]%, P<0.05). Comprehensively, the natural sedimentation method is the best option. The ex vivo expansion fold of T cells in IL-2 group was significantly higher than that in mixed group ([262.6±143.2] times vs [73.0±25.8] times, P<0.05). The proportions of early memory T cells, Tscm+Tscm-like and Tcmin the mixed group were significantly higher than those in the IL-2 group ([55.6±1.82]% vs [39.6±1.52]%, [16.6±1.82]% vs [9.8±1.30]%, [39.0±1.58]% vs [29.2±1.79]%; all P < 0.05). Conclusion: : Natural sedimentation sorting has advantages of low cost, high recovery and purity. Mixed cytokines of IL-7, IL-15 and IL-21 are beneficial for production of early memory T cells. This study provides an experimental data of ex vivo T cell preparation for cancer adoptive immunotherapy.
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@#[Abstract] Objective:To investigate whether the proliferation and cytotoxicity of NK-92MI cells can be improved by IL-7 and IL-21 genes modification, and determine the effects of this genetically modified NK-92MI cells on T cells from normal human peripheral blood. Methods:IL-7 and IL-21 gene fragments were constructed into electroporation vector by genetic engineering method, and NK92MI/IL-21 and NK-92MI/IL-7&21 cells were constructed by electroporation transfection. The in vitro proliferation and cytotoxicity of NK-92MI, NK-92MI/IL-21 and NK-92MI/IL-7&21 cells were measured by cell count and flow cytometry assays. Then, normal human PBMCs were co-cultured with NK-92MI, NK-92MI/IL-21 and NK-92MI/IL-7&21 cells in vitro respectively, and the phenotype change of T cells was measured by flow cytometry. In addition, the cytotoxicity between the activated T cells and three NK-92MI cell lines (NK-92MI, NK-92MI/IL-21 and NK-92MI/IL-7&21 cells) as well as the cytotoxicity of the three NK-92MI cells on tumor cells after co-incubation with activated T cells were detected. Results: NK-92MI/IL-21 cell line (highly expressing IL-21) and NK-92MI/IL-7&21 cell line (highly expressing both IL-7 and IL-21) were successfully constructed. The toxicity of NK-92MI, NK-92MI/IL-21 and NK92MI/IL-7&21 cells on Jurkat and K562 cells showed no difference, while the proliferation of NK-92MI/IL-21 and NK-92MI/IL-7&21 cells was increased compared with NK-92MI cells. Furthermore, NK-92MI/IL-21 and NK-92MI/IL-7&21 cells promoted the activation of T cells to a certain degree, and the activated T cells showed merely no cytotoxicity on NK-92MI, NK-92MI/IL-21 and NK-92MI/IL7&21 cells; Meanwhile, the activated T cells did not affect the cytotoxicity of the three NK cells (NK-92MI, NK-92MI/IL-21, and NK92MI/IL-7&21 cells) on K562 cells under their co-existence. Conclusion: The in vitro proliferation of NK-92MI/IL-21 and NK-92MI/ IL-7&21 cells were enhanced after gene modification, which could also stimulate and promote the activation of T cells from peripheral blood. The cytotoxicity assay showed that the activated T cells had no cytotoxicity on NK-92MI, NK-92MI/IL-21, and NK-92MI/IL-7& 21 cells. Meanwhile, the presence of the activated T cells did not affect the cytotoxicity of NK-92MI cells.
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Herpes zoster (HZ), or shingles, is caused by the reactivation of latent varicella-zoster virus (VZV) from the sensory ganglia when VZV-specific T-cell immunity is decreased because of aging or immunosuppression. In the present study, we developed HZ DNA vaccine candidates encoding VZV proteins and cytokine adjuvants, such as IL-7 and IL-33. We immunized C57BL/6 mice with DNA plasmids encoding VZV glycoprotein E (gE), immediate early (IE) 63, or IE62 proteins and found that robust VZV protein-specific T-cell responses were elicited by HZ DNA vaccination. Co-administration of DNA plasmids encoding IL-7 or IL-33 in HZ DNA vaccination significantly enhanced the magnitude of VZV protein-specific T-cell responses. Protective immunity elicited by HZ DNA vaccination was proven by challenge experiments with a surrogate virus, vaccinia virus expressing gE (VV-gE). A single dose of HZ DNA vaccine strongly boosted gE-specific T-cell responses in mice with a history of previous infection by VV-gE. Thus, HZ DNA vaccines with IL-7 and IL-33 adjuvants strongly elicit protective immunity.
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Animales , Ratones , Envejecimiento , ADN , Ganglios Sensoriales , Glicoproteínas , Herpes Zóster , Herpesvirus Humano 3 , Terapia de Inmunosupresión , Interleucina-33 , Interleucina-7 , Plásmidos , Linfocitos T , Vacunación , Vacunas de ADN , Virus VacciniaRESUMEN
Despite the widespread use of proteasome inhibitors in the treatment of multiple myeloma, the mechanisms of the anti-myeloma activity and the molecular pathways that execute the tumor cell killing are still unknown. In the present work we compared gene expression profile changes in response to bortezomib treatment of cultured bone marrow samples from patients with bortezomibsensitive versus bortezomib-resistant myeloma. The results showed a pronounced induction of>70 genes including>30 heat shock protein transcripts in both patient groups and therefore debate the anti-tumor action, attributed to the unfolded protein response. In contrast, a subset of 7 genes (MMP12, IL7R, MGST1, C3, CYP27A1, MIR148A and CXXC4) changed only in the samples from the bortezomib-sensitive cases and therefore these tumor-associated genes might serve as predictors of the treatment efficacy, as well as for making of further insights onto the mechanism of action of proteasome inhibitors. In summary, we identified a subset of 7 genes which distinguished in our small series betweensensitive versus resistant tumor cells to bortezomib, which requires further assessment in a larger cohort of patients.
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Background& objectives: Metabolic syndrome (MS) is a common but serious public health problem in developed countries. Chronic inflammation plays a key role in MS. Interleukins (IL)-7 and 8 are considered to have proinflammatory effects and may be involved in the pathogenesis of MS. Therefore, the aim of this study was to determine gene expression level of IL-7 and IL-8 in peripheral blood mononuclear cells (PBMCs) of patients with MS compared to healthy control subjects. Methods: Using real-time RT-PCR, the relative amounts of IL-7 and IL-8 mRNA were determined in PBMCs from 20 female patients with MS and compared with those of 20 healthy control subjects. Biochemical and anthropometric parameters of MS were also assessed. Results: Total cholesterol, triglyceride, and fasting blood sugar were significantly higher in MS patients compared to healthy subjects. There were no significant differences in HDLc and LDLc between the two groups. IL-8 expression in PBMC was significantly decreased in MS versus control subjects (fold of change was 0.395 ± 0.1824), while no difference in the IL-7 expression was detected between them. IL-8 expression had negative correlation with MS components especially with triglyceride and total cholesterol (r=0.5, P<0.001). Interpretation & conclusions: In this preliminary study, no detectable differences were found in IL-7 expression and decreased expression of IL-8 in PBMCs of MS patients as compared to those of control subjects. Study on a larger population and investigating the mechanisms involved can reveal more details.
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Aim: The aim of this study was to examine whether a Human herpes virus-6 (HHV-6) infection increases the risk of MS in individuals harboring particular cytokine receptor α- chain gene alleles. Study Design: MS patients and controls were assessed for HHV-6 DNA and for single nucleotide polymorphisms (SNPs) in their IL7RA and IL2RA genes. Place and Duration of Study: The study was carried out at the Department of Experimental Pathology, Microbiology and Immunology, American University of Beirut, between March 2011 and March 2013. Methodology: Blood samples from 100 MS patients and 100 controls were investigated for the presence of HHV-6 by nested PCR. Single nucleotide polymorphisms (SNPs) in the IL7RA and IL2RA genes were examined by restriction fragment length polymorphism. Results: HHV-6 was detected in 58% of MS patients and 32% of controls (OR = 2.935, 95% CI = 1.582-5.463, p=0.000). We did not detect a statistically significant correlation between MS and the studied rs2104286, rs12722489 SNPs in the IL2RA gene and rs6897932 SNP in the IL7RA gene. Concomitant presence of rs2104286 and HHV-6 was detected in 56% of patients and 30% of controls (OR=2.970, 95% CI=1.594-5.53, P=0.000). Similarly, rs6897932 and HHV-6 were observed in 57% of patients and 28% of controls (OR=3.409, 95% CI= 1.815-6.428, P=0.000). Therefore, double positivity moderately increased the risk of MS compared to either factor alone. HHV-6 and rs12722489 double positivity did not increase the risk of MS. Conclusion: HHV-6 infections may enhance the risk of MS in subjects with particular genetic determinants.
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Objective:To explore a new method of the cultivation of adoptive immunotherapy cells.Methods: Mononuclear cells was isoplated by density gradient centrifugation and then proliferated by using CD 40-agonist monoclonal antibody 5C11、cytokine of IFN-αand IL-7(CD40 group)in vitro.During the culturing procedure ,the cell morphology was obersved by optical microscope.The percentage of T-lymphocytes, NK-T cells, Treg cells and the cell proliferation, which were compared with CIK group CD3mAb activated,was detected on the 9th day.Results:There was no significant difference of CD 4+/CD8+T cells percentage between the two groups.But the Treg cells percentage of CIK group was far higher than that of CD 40 group,while the percentage of CD3+CD56+NK-T cells was lower than that of CD 40 group.And a group of Mo-NK-DC cells were observed in the CD 40 group.Conclusion: The new method of adoptive immunity therapy has been established in this study could increase the percentage of NK -T cells which had the ability to kill tumor cells.Simultaneously ,it is reduced the amount of Treg cells significantly.
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Objective:To explore the promoting effects of IL-7 and IL-2 on CD4+CD25-T cells proliferation in vitro and construct a stable culture system in vitro for CD 4+CD25+regulatory T cells from human umbilical cord blood.To compare the inhibiting effects between induced proliferated CD 4+CD25+Tregs and naturally isolated CD 4+CD25+Tregs on PBMCs functional activity.Methods:CD4+CD25-T cells and CD4+CD25+T cells were isolated from human umbilical cord blood mononuclear cells by magnetic activated cell sorting ( MACS) system and then expanded in vitro.Four different concentration levels of IL-7 combined with proper concentration of IL-2 were added as inducer and the efficiency and optimal concentration of IL-7 on inducing,CD4+CD25-T cells were analyzed via 4 different methods.Flow cytometry method was used to detect the changes of CD 4+CD25-T cells.The inhibitory effect of expanded CD 4+CD25+T cells on peripheral blood mononuclear cells (PBMCs) was tested by MTS.The expressions of Foxp3,IL-10 and TGF-βgenes in CD4+CD25+T cells were test by RT-PCR.Results:The CD4+CD25+T cells from each groups were expanded significantly after three weeks of culture.The results indicated that use of IL-7 combined with IL-2 resulted in the highest cell expansion comparing to the other groups.It was shown by the inhibitory test that the expanded CD 4+CD25+regulatory T cells could inhibit the proliferation of PBMCs ,but IL-7 induced CD4+CD25+regulatory T cells exerted weaker suppressor activity than natural regulatory T cells .Only IL-7 (4 ng/ml) and IL-2 (2 000 U/ml) induced CD4+CD25+regulatory T cells showed the strongest killing activity.Conclusion:We successfully expand CD4+CD25+regulatory T cells in vitro.The protocol is established in which the use of mAbCD 3/CD28 combined with IL-7 and IL-2 resulted in the highest cell expansion ,and intensely expressed cell phenotype of CD 4 and CD25.
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Objective To examine the therapeutic effect of C Ⅱ TA inhibition in collagen-induced arthritis(CIA),using a delivery system tailored to target C ⅡTA gene by small interfering RNA (siRNA).Methods Mice with collagen-induced arthritis were injected intravenously with C Ⅱ TA siRNA.The clinical score was monitored for up to 4 weeks after treatment.The severity of inflammation of mouse joint was evaluated by histological examination.Real-time PCR was used to determine the cytokine mRNA expression.Cytokine production was measured by ELISA from serum.T cell proliferation was examined by MTT method.Results IFN-γ and IL-17 were elevated in CIA mice,but were iuhibited significantly by C Ⅱ TA siRNA either prevention or intervention of autoimmune arthritis.Collagen specific T cell proliferation was significantly suppressed.Increased level of IL-4 by T cells was observed in C Ⅱ TA siRNA treated group compared with that of control group.Conclusion Our findings indicate that systemic RNAi-mediated C Ⅱ TA gene silencing is effective in the treatment of CIA and regulateds the balance of Th1/Th2 differentiation.
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BACKGROUND: A crucial limitation of DNA vaccines is its weak immunogenicity, especially in terms of eliciting antibody responses in non-human primates or humans; therefore, it is essential to enhance immune responses to vaccination for the development of successful DNA vaccines for humans. METHODS: Here, we approached this issue by evaluating interleukin-7 (IL-7) as a genetic adjuvant in cynomolgus monkeys immunized with multigenic HCV DNA vaccine. RESULTS: Codelivery of human IL-7 (hIL-7)-encoding DNA appeared to increase DNA vaccine-induced antibody responses specific for HCV E2 protein, which plays a critical role in protecting from HCV infection. HCV-specific T cell responses were also significantly enhanced by codelivery of hIL-7 DNA. Interestingly, the augmentation of T cell responses by codelivery of hIL-7 DNA was shown to be due to the enhancement of both the breadth and magnitude of immune responses against dominant and subdominant epitopes. CONCLUSION: Taken together, these findings suggest that the hIL-7-expressing plasmid serves as a promising vaccine adjuvant capable of eliciting enhanced vaccine-induced antibody and broad T cell responses.
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Humanos , Formación de Anticuerpos , ADN , Interleucina-7 , Macaca fascicularis , Plásmidos , Primates , Vacunación , Vacunas de ADNRESUMEN
CD127 is the interleukin7 receptor ?(IL7R?),it regulates the specific respond of T lymphocytes to IL7.CD127 plays an indispensable role in the development of thymocytes into T lymphocytes,the survival and homeostatic proliferation of memory T cells.There are only two phases of the life period of T cells that do not express CD127:immature CD4+8+double positive(DP)thymocytes and activated T cells.Recently,it was found that CD127 play an important role as the specific marker of memory T cells and regulator T cells.The role and mechanism of CD127 in the life period of T cells were discussed herein.
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BACKGROUND: Interleukin-7 receptor (IL-7R) alpha-deficient mice have small numbers of B cells and alpha beta T cells in periphery, they totally lack gamma sigma T cells. In addition, the V-J recombination and transcription of TCRgamma genes is also severely impaired in IL-7Ralpha-deficient mice. Stat5, a signaling molecule of the IL-7R, induces germline transcription in the TCRgamma locus, and promotes V-J recombination and gamma sigma T cell development. However, the roles for IL-7R signaling pathway in thymic or extrathymic gamma sigma T cell development are largely unknown. METHODS: To clarify the role of the IL-7 receptor in proliferation and survival of gamma sigma T cells, we introduced the TCR gamma sigma transgene, Vgamma2/ Vsigma5, into IL-7Ralpha-deficient mice, and investigated the development of gamma sigma T cells. RESULTS: We found that Vgamma2/Vsigma5 transgene restored gamma sigma T cells in the epithelium of the small intestine (IEL) but not in the thymus and the spleen. Further addition of a bcl-2 transgene resulted in partial recovery of gamma sigma T cells in the thymus and the spleen of these mice. CONCLUSION: Taken together, this study revealed that the IL-7Ralpha is indispensable for proliferation and survival mainly in thymic gamma sigma T cell development.
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Animales , Ratones , Linfocitos B , Epitelio , Interleucina-7 , Intestino Delgado , Receptores de Interleucina-7 , Recombinación Genética , Bazo , Linfocitos T , Timo , TransgenesRESUMEN
Objective:To investigate the expression of interleukin-7 in human liver and stomach,identify the splice variants of IL-7.Methods:Reverse transcription-polymerase chain reaction(RT-PCR) was used for investigating the expression of IL-7.According to IL-7 gene cDNA,the primers were designed and synthesized,then the splice variants of IL-7 in human cancer tissues was identify,cloned into vector and sequenced.Results:The results showed that(1)the expression of IL-7 mRNA was nearly equal between human liver and stomach,(2)two new bands of IL-7 was obtained from liver cancer and gastric carcinoma,one lacks exon 4,another exon 5.Conclusion:IL-7 gene is expressed highly in both human liver and stomach.In addition,human liver cancer and gastric carcinoma can produce splicing variants of IL-7 by alternative splicing.