We have studied the function of lymphokines on human tonsillar B cell prolifertion and differentiation. B cells were stimulated with Staphylococcus aureus Cowanl (SAC) or anti- bead. The followings showed the results of this study. 1) In B cell activation, SAC induced B cell DNA synthesis but anti-mubead did not. SAC could activate and proliferate B cells. Minimal number of B cells were required to proliferate effectively. 2) In B cell proliferation, SAC could proliferate B cell in the abscence of lymphokines. Exogenous IL-2 or IL-4 enhanced B cell proliferation. The roles of IL-2 were very important in B cell proliferation. The effect of IL-4 on the IL-2 induced B cell proliferation was inhibitory in SAC-B cells. IL-4 could enhance the proliferation of anti-mu bead activated B cells. 3) In B cell differentiation, IL-2 was a major factor to differentiate SAC activated B cells, but IL-4 did not. IL-6 had a synergistic effect on the differentiation. The results of this study showed that the different signal transduction mechanisms were involved in B cell proliferation and differentiation. The B cell resposes to lymphokine were different, and it is depend upon antigens or mitogens.
B-Lymphocytes ; Cell Differentiation ; Cell Proliferation* ; DNA ; Humans* ; Interleukin-2 ; Interleukin-4 ; Interleukin-6 ; Lymphokines ; Mitogens ; Signal Transduction ; Staphylococcus aureus

Intravesical Bacillus Calmette-Guerin (BCG) therapy is an effective immunotherapy used for the treatment and prophylaxis of superficial bladder cancer. The mechanism through which BCG exerts its antitumor activity is not fully understood. However, several studies suggest that antitumor mechanism of BCG is associated with T-cell mediated immunity and lymphokines. In this report, the detection of IL-2(a lymphokine produced in response to BCG) in urine and serum specimens of patients treated with intravesical BCG is reported. Urine specimens of 10 superficial bladder cancers were obtained prior to BCG instillation, 4, 8, and 24 hours afterwards. Serum specimens of same patients were obtained before and 8 hours after BCG instillation. No change of serum IL-2 before and after BCG instillation were observed. Urinary IL-2 production increased significantly 4 and 8 hours (p<0.05) and decreased 24 hours after BCG instillation. Urinary IL-2 levels 24 hours after BCG instillation were similar to baseline values. Between urinary IL-2 of healthy men and cystitis patients were similar. These results suggest that BCG induce IL-2 production with highest level at 4 hours after BCG instillation and IL_2 might play a important role in antitumor mechanism of BCG. However, further studies are necessary to elucidate the antitumor mechanism of BCG.
Bacillus ; Cystitis ; Humans ; Immunotherapy ; Interleukin-2* ; Interleukins* ; Lymphokines ; Male ; Mycobacterium bovis* ; T-Lymphocytes ; Urinary Bladder Neoplasms* ; Urinary Bladder*

This study was undertaken to investigate the immunological mechanism of Behqet s syndrome, considered to be important in the pathogenesis of the disease. Seventy- three patients with complete, incomplete and suspected types of Behget's syndrotne were tested for leukocyte migration ingibition factor(LIF), one of the lymphokines. The results were as follows : 1. There was no difference between the average LIF activity of all the patients and that of eontrol. 2. LIF activity of complete type, according to Shirnizus classification, was significaritly lower than the control value. 3. LIF activity of ocular type, according to Lehners classification, was signficantly lower than the control value. 4. LIF activity for patients with 4 clinical symptoms was well below the value for patients with less symptomes 5. For patients with single clinical symptom, LIF activity of complete type was well below the values of incomplete and suspected types. 6. In suspected and mucocutaneous types, LIF activity was low when the patients showed two clinical symptoms than one. Thus, LIF activity was low for patients with complete, ocular and neurological types and with multiple symptorns.
Behcet Syndrome* ; Classification ; Humans ; Leukocytes* ; Lymphokines

No abstract available.
Humans* ; Lymphokines* ; Monocytes* ; Mycobacterium tuberculosis* ; Mycobacterium*

BACKGROUND: It has been demonstrated that patients with atopic dermatitis(AD) show an impaired capacity of their T cells to release of interleukin-2(IL-2) in vitro and elevated serum levels of soluble IL-2 receptor(sIL-2R). Both immunosuppressive agents, cyclosporin A(CsA) and FK-506 can block early events in T lymphocyte activation and FK-506 is 10- to 100-fold more potent in the inhibition of IL-2 and other lymphokines production. OBJECTIVE: We compared the effects of CsA and FK-506 on PHA-induced lymphokine and sIL-2R production and compared the effects of CsA and FK-506 on PHA-induced IL-4 production in a high IgE group and a low IgE group in patients with AD. METHODS: A total of 32 peripheral blood samples from 17 patients with AD and 15 control groups were tested. Lymphocytes were isolated from blood samples and were cultured with PHA(positive control), PHA and CsA(10 ng/ml), PHA and FK-506 (1 ng/ml), and without stimulation (negative control). The amount of cytokines such as IL-2, IL-3, IL-4 and sIL-2R were measured using an enzyme-linked immunosorbent assay(ELISA). RESULTS: CsA and FK-506 inhibited significantly the production of IL-2, IL-3, IL-4 in PHA-stimulated lymphocytes of both the AD patients and the control groups. FK-506(1 ng/ml) inhibited cytokines production more significantly than CsA(10 ng/ml). However, CsA and FK-506 did not significantly inhibit the production of sIL-2R. There were no significant differences in the inhibitory effect of CsA and FK-506 on IL-4 production upon PHA-stimulation between AD patients with a high IgE level and with a low IgE level. CONCLUSION: Both FK-506 and CsA inhibit lymphokine production, but not the production of sIL-2R. FK-506 inhibited more significantly lymphokine production at a 10-fold lower concentration than CsA. Our data suggest that FK-506 could be more effective in the treatment of severe AD than CsA, and both these agents show their immunosuppressive activity through the suppression of lymphokine production, not via the suppression of sIL-2R production in AD.
Cyclosporine* ; Cytokines ; Dermatitis, Atopic* ; Humans ; Immunoglobulin E ; Immunosuppressive Agents ; In Vitro Techniques ; Interleukin-2 ; Interleukin-3 ; Interleukin-4 ; Lymphocyte Activation ; Lymphocytes* ; Lymphokines ; T-Lymphocytes ; Tacrolimus*

OBJECTIVETo construct the adenoviral vector bringing hVEGF(121) cDNA for evaluation of the possibility of VEGF gene therapy in ischemic bone disease.

METHODSHuman vascular endothelial growth factor (hVEGF(121)) cDNA obtained from the plasmid pCDI/VEGF(121) was cloned into plasmid pshuttle and further cloned to Adeno-X Viral DNA. The recombinant adenoviral plasmid was identified and then transferred to the adenoviral packaging cell HEK293 by lipofectamine mediated gene transfer method to pack the virus. After titilating the virus, the mouse bone marrow stromal cells (MSC) were transfected by the adenovirus and the expression of VEGF gene was detected.

RESULTSThe recombinant Adeno-VEGF(121) was correctly constructed and confirmed by restriction endonuclease analysis and DNA sequencing analysis. After MSCs were tranfected by the virus, RT-PCR showed that hVEGF(121) mRNA was transcripted from the hVEGF(121) gene. Western blot and immune histochemistry showed VEGF(121) protein was expressed in transgene MSCs.

CONCLUSIONThe recombinant adenoviral vector bringing hVEGF(121) cDNA was successfully constructed and the transgene MSC expressed hVEGF gene in vitro, it provided the further foundation of VEGF gene therapy for bone ischemic diseases.

Adenoviridae ; genetics ; Blotting, Western ; Cells, Cultured ; DNA, Complementary ; genetics ; Endothelial Growth Factors ; genetics ; metabolism ; Gene Expression ; Gene Transfer Techniques ; Genetic Vectors ; genetics ; Humans ; Immunohistochemistry ; Lymphokines ; genetics ; metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors

OBJECTIVETo investigate the feasibility of endothelialization of bioprosthesis by transfer of vascular endothelial growth factor (VEGF) gene.

METHODSBovine pericardium treated with glutaraldehyde and L-glutamic acid was positioned into the pig right atrium. pcD(2)/hVEGF(121) gene (1 mg) was transferred into the right ventricular myocardium using surgical sutures Reverse transcri ption polymerase chain reaction (RT PCR) was employed to evaluate the expression of myocardial VEGF mRNA. The determination of concentrations of VEGF protein in blood from both the right atrium and peripheral vein, and histological and ultrastructural analysis of implanted bovine pericardium were completed simultaneously.

RESULTSThe concentration of VEGF derived from the right atrium in pcD(2)/hVEGF(121) group was significantly higher than that in the pcD(2) group 10 days after VEGF gene transfer (P < 0.01). The expression of myocardial VEGF mRNA in pcD(2)/hVEGF(121) group was much higher in comparison with that in the pcD(2) group. The morphological analysis demonstrated that the coverage rate of host endothelium in the pcD(2)/hVEGF(121) group was 2.6 times as fast as that in the pcD(2) group at 16 days after VEGF(121) gene transfer (P < 0.01). Entire endothelialization occurred at 30 days after VEGF gene transfer. In addition, higher expression of myocardial VEGF mRNA was still available.

CONCLUSIONSVEGF gene transfer by surgical suture can remarkably accelerate endothelialization of bioprosthesis, which may provide a new approach for inhibiting biological valve calcification and improve biocompatibility and long-term durability of the bioprosthesis.

Animals ; Bioprosthesis ; Endothelial Growth Factors ; analysis ; genetics ; Endothelium, Vascular ; physiology ; Female ; Gene Transfer Techniques ; Heart Valve Prosthesis ; Humans ; Lymphokines ; analysis ; genetics ; Male ; RNA, Messenger ; analysis ; Swine ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors

OBJECTIVETo investigate the killing effect of herpes simplex virus thymidine kinase gene expression actuated by the promoter of the vascular endothelial growth factor gene on human hepatocellular tumor cells under hypoxic condition.

METHODSRecombinant adenoviral vectors, AdVEGF-tk and AdVEGF-GFP, were constructed with HSV-tk or GFP under the control of VEGF promoter through AdEasy system. Then GFP expression in hepatoma cell line HepG2 and normal liver cell line L02 transfected with AdVEGF-GFP were observed under fluorescence microscope, and the sensitivity to GCV of the AdVEGF-tk-transfected cells under normoxia or hypoxia condition were monitored by MTT method.

RESULTSGFP expression actuated by VEGF promoter was detected in sporadic L02 cells, but in almost all HepG2 cells after transfected with AdVEGF-GFP. With GCV at 10 micro g/ml and MOI at 100, L02 cells were insensitive to GCV under oxic condition, but more than 70% L02 cells were killed under hypoxic condition. Moreover, HepG2 cells infected with AdVEGF-tk showed the increased GCV sensitivity under hypoxia (over 80% killed) as compared with normoxia (over 60% killed) conditions.

CONCLUSIONHypoxia enhances the GCV sensitivity of human hepatocellular tumor cells infected with recombinant AdVEGF-tk under the control of VEGF promoter.

Adenoviridae ; genetics ; Carcinoma, Hepatocellular ; pathology ; Endothelial Growth Factors ; genetics ; Gene Expression ; drug effects ; Gene Transfer Techniques ; Genetic Vectors ; genetics ; Humans ; Hypoxia ; Intercellular Signaling Peptides and Proteins ; genetics ; Liver Neoplasms ; pathology ; Lymphokines ; genetics ; Oxygen ; pharmacology ; Promoter Regions, Genetic ; physiology ; Simplexvirus ; enzymology ; Thymidine Kinase ; genetics ; metabolism ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors

The purpose of this preliminary study is to elucidate that vascular endothelial growth factor (VEGF) influences contrast enhancement of hepatic tumors on computed tomography (CT). Fourteen patients with hepatic tumors (11 hepatocellular carcinomas; 3 metastatic cancers) underwent a dual-phase dynamic helical CT or computed tomographic hepatic arteriography. The attenuation of each mass was determined as hyperattenuation, isoattenuation or hypoattenuation with respect to the adjacent nontumorous parenchyma. Gun-needle biopsy was done for each tumor, and paraffin sections were immunostained with anti- VEGF antibody by the avidin-biotin-peroxidase complex method. The pathologic grade was made by intensity (1 +, 2+, 3+) and area (+/-, 1 +, 2+). The tumor ranged 2.0-14.0 cm in size (mean, 5.8 cm). In arterial phase, the intensity was not correlated with the degree of enhancement (p=0.086). However, the correlation between the attenuation value of hepatic arterial phase and the area of positive tumor cells was statistically significant (p=0.002). VEGF may be the factor that enhances the hepatic mass with water-soluble iodinated contrast agent in CT.
Adult ; Aged ; Capillary Permeability ; Endothelial Growth Factors/physiology* ; Endothelial Growth Factors/analysis ; Female ; Human ; Liver Neoplasms/radiography* ; Liver Neoplasms/blood supply ; Lymphokines/physiology* ; Lymphokines/analysis ; Male ; Middle Age ; Prospective Studies ; Radiographic Image Enhancement* ; Tomography, X-Ray Computed

A secondary aortoenteric fistula (AEF) is a direct communication between the gastrointestinal tract and the aorta in a patient who has undergone major surgery on the aorta, often an aorta graft operation. We experienced a patient who had undergone graft interposition for abdominal aortic aneurysm and was admitted due to three episodes of hematemesis and following hamatochezia. Gastroscopy, colonoscopy, and radioactive iodine scan failed to identify the bleeding site in the patient. He was diagnosed with AEF by double balloon enteroscopy and recovered after surgical intervention.
Aorta ; Aortic Aneurysm, Abdominal ; Colonoscopy ; Double-Balloon Enteroscopy ; Fistula ; Gastrointestinal Tract ; Gastroscopy ; Hematemesis ; Hemorrhage ; Humans ; Iodine ; Lymphokines ; Transplants