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Immunomodulatory Effects of ZYM-201 on LPS-stimulated B Cells.

Ye Eun LEE ; Soochan KIM ; Woong Jae JUNG ; Hyung Soo LEE ; Mi Yeon KIM

Immune Network.2014;14(5):260-264. doi:10.4110/in.2014.14.5.260

ZYM-201 is a methyl ester of triterpenoid glycoside from Sanguisorba officinalis which has been used for treatment of inflammatory and metabolic diseases. In this study, immunomodulatory effects of ZYM-201 on B cells were examined in vitro and in vivo. When splenocytes were activated with lipopolysaccharide (LPS), the major population which had shown an increase in cell numbers was B cells. However, when the B cells were treated with ZYM-201 after LPS activation, their cell numbers and the expression of major costimulatory molecules, CD80 and CD86, were decreased. Furthermore, the effect of LPS, which induces activation of NF-kappaB, was abolished by ZYM-201: LPS-stimulated B cells showed decrease of phosphorylation after treatment of ZYM-201. The same results were shown in vivo experiments. These results suggest that ZYM-201 may play a role in the modulation of inflammatory responses through inhibiting NF-kappaB activation and downregulating the expression of costimulatory molecules on B cells.
B-Lymphocytes* ; Cell Count ; Inflammation ; Metabolic Diseases ; NF-kappa B ; Phosphorylation ; Sanguisorba

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Effects of Endurance Training on the Serum Levels of Tumour Necrosis Factor-alpha and Interferon-gamma in Sedentary Men.

Abdolreza Sotoodeh JAHROMI ; Abdossaleh ZAR ; Fatemeh AHMADI ; Peter KRUSTRUP ; Khosrow EBRAHIM ; Friborz HOVANLOO ; Davar AMANI

Immune Network.2014;14(5):255-259. doi:10.4110/in.2014.14.5.255

Physical activity could be considered one of the factors that affect the immune system status and function. To find the relation between exercise and cytokines, we examined the possible effects of an 8-week endurance training program on the serum levels of cytokines, including tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in sedentary men. A total of 30 healthy young male volunteers were randomly divided into an endurance training group and a control group. The training group followed a specific exercise protocol (running on a treadmill for 15~30 min at 50~70% maximal heart rate) for 8 weeks and the control group did not participate in any exercise program. Venous blood samples were collected from both the groups 24 h before and 24 h and 48 h after the exercise. Repeated ANOVA was used for statistical purposes. The serum levels of TNF-alpha and IFN-gamma were determined by ELISA. Significant (p<0.05) and non-significant (p>0.05) decreases were observed in the serum levels of IFN-gamma and TNF-alpha, respectively, after the 8-week endurance training program. Our findings indicated that an 8-week endurance exercise may affect the serum levels of some inflammatory cytokines, suggesting the beneficial role of this training protocol in elderly population and people with certain conditions (inflammation of the vertebrae or other inflammatory diseases).
Aged ; Cytokines ; Education ; Enzyme-Linked Immunosorbent Assay ; Heart ; Humans ; Immune System ; Interferon-gamma* ; Male ; Motor Activity ; Necrosis* ; Spine ; Tumor Necrosis Factor-alpha ; Volunteers

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A Novel Translocation Involving RUNX1 and HOXA Gene Clusters in a Case of Acute Myeloid Leukemia with t(7;21)(p15;q22).

Yeonsook MOON ; Douglas E HORSMAN ; R Keith HUMPHRIES ; Gyeongsin PARK

Immune Network.2013;13(5):222-226. doi:10.4110/in.2013.13.5.222

Translocations involving chromosome 21q22 are frequently observed in hematologic malignancies including acute myeloid leukemia (AML), most of which have been known to be involved in malignant transformation through transcriptional dysregulation of Runt-related transcription factor 1 (RUNX1) target genes. Nineteen RUNX1 translocational partner genes, at least, have been identified, but not Homeobox A (HOXA) genes so far. We report a novel translocation of RUNX1 into the HOXA gene cluster in a 57-year-old female AML patient who had been diagnosed with myelofibrosis 39 months ahead. G-banding showed 46,XX,t(7;21)(p15;q22). The involvement of RUNX1 and HOXA genes was confirmed by fluorescence in situ hybridization.
Core Binding Factor Alpha 2 Subunit ; Female ; Fluorescence ; Genes, Homeobox ; Hematologic Neoplasms ; Humans ; In Situ Hybridization ; Leukemia, Myeloid, Acute* ; Middle Aged ; Multigene Family* ; Primary Myelofibrosis

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B Cells Promote Th1- Skewed NKT Cell Response by CD1d-TCR Interaction.

Jung Hoon SHIN ; Se Ho PARK

Immune Network.2013;13(5):218-221. doi:10.4110/in.2013.13.5.218

CD1d expressing dendritic cells (DCs) are good glyco-lipid antigen presenting cells for NKT cells. However, resting B cells are very weak stimulators for NKT cells. Although alpha-galactosylceramide (alpha-GalCer) loaded B cells can activate NKT cells, it is not well defined whether B cells interfere NKT cell stimulating activity of DCs. Unexpectedly, we found in this study that B cells can promote Th1-skewed NKT cell response, which means a increased level of IFN-gamma by NKT cells, concomitant with a decreased level of IL-4, in the circumstance of co-culture of DCs and B Cells. Remarkably, the response promoted by B cells was dependent on CD1d expression of B cells.
Antigen-Presenting Cells ; B-Lymphocytes* ; Coculture Techniques ; Dendritic Cells ; Galactosylceramides ; Interleukin-4 ; Natural Killer T-Cells*

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Bacteroides fragilis Toxin Induces IL-8 Secretion in HT29/C1 Cells through Disruption of E-cadherin Junctions.

Soonjae HWANG ; Sun Yeong GWON ; Myung Sook KIM ; Seunghyung LEE ; Ki Jong RHEE

Immune Network.2013;13(5):213-217. doi:10.4110/in.2013.13.5.213

Enterotoxigenic Bacteroides fragilis (ETBF) is a human gut commensal bacteria that causes inflammatory diarrhea and colitis. ETBF also promotes colorectal tumorigenesis in the Min mouse model. The key virulence factor is a secreted metalloprotease called B. fragilis toxin (BFT). BFT induces E-cadherin cleavage, cell rounding, activation of the beta-catenin pathway and secretion of IL-8 in colonic epithelial cells. However, the precise mechanism by which these processes occur and how these processes are interrelated is still unclear. E-cadherin form homophilic interactions which tethers adjacent cells. Loss of E-cadherin results in detachment of adjacent cells. Prior studies have suggested that BFT induces IL-8 expression by inducing E-cadherin cleavage; cells that do not express E-cadherin do not secrete IL-8 in response to BFT. In the current study, we found that HT29/C1cells treated with dilute trypsin solution induced E-cadherin degradation and IL-8 secretion, consistent with the hypothesis that E-cadherin cleavage causes IL-8 secretion. However, physical damage to the cell monolayer did not induce IL-8 secretion. We also show that EDTA-mediated disruption of E-cadherin interactions without E-cadherin degradation was sufficient to induce IL-8 secretion. Finally, we determined that HT29/C1 cells treated with LiCl (beta-catenin activator) induced IL-8 secretion in a dose-dependent and time-dependent manner. Taken together, our results suggest that BFT induced IL-8 secretion may occur by the following process: E-cadherin cleavage, disruption of cellular interactions, activation of the beta-catenin pathway and IL-8 expression. However, we further propose that E-cadherin cleavage per se may not be required for BFT induced IL-8 secretion.
Animals ; Bacteria ; Bacterial Toxins ; Bacteroides fragilis* ; Bacteroides* ; beta Catenin ; Cadherins* ; Cell Transformation, Neoplastic ; Colitis ; Colon ; Diarrhea ; Edetic Acid ; Epithelial Cells ; Fibrinogen ; Humans ; Interleukin-8* ; Metalloendopeptidases ; Mice ; Trypsin

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Dectin-1 Stimulation Selectively Reinforces LPS-driven IgG1 Production by Mouse B Cells.

Beom Seok SEO ; Sang Hoon LEE ; Ju Eon LEE ; Yung Choon YOO ; Junglim LEE ; Seok Rae PARK

Immune Network.2013;13(5):205-212. doi:10.4110/in.2013.13.5.205

Dectin-1, which specifically recognizes beta-glucan of fungal cell walls, is a non-Toll-like receptor (TLR) pattern recognition receptor and a representative of C-type lectin receptors (CLRs). The importance of Dectin-1 in innate immune cells, such as dendritic cells and macrophages, has previously been well studied. However, the function of Dectin-1 in B cells is very poorly understood. To determine the role of Dectin-1 in B cell activation, we first investigated whether mouse B cells express Dectin-1 and then assessed the effect of Dectin-1 stimulation on B cell proliferation and antibody production. Mouse B cells express mRNAs encoding CLRs, including Dectin-1, and surface Dectin-1 was expressed in B cells of C57BL/6 rather than BALB/c strain. Dectin-1 agonists, heat-killed Candida albicans (HKCA) and heat-killed Saccharomyces cerevisiae (HKSC), alone induced B cell proliferation but not antibody production. Interestingly, HKSC, HKCA, and depleted zymosan (a selective Dectin-1 agonist) selectively enhanced LPS-driven IgG1 production. Taken together, these results suggest that, during fungal infection, beta-glucan-stimulated Dectin-1 may cooperate with TLR4 to specifically enhance IgG1 production by mouse B cells.
Animals ; Antibody Formation ; B-Lymphocytes* ; Candida albicans ; Cell Proliferation ; Cell Wall ; Dendritic Cells ; Immunoglobulin G* ; Lectins, C-Type ; Macrophages ; Mice* ; RNA, Messenger ; Saccharomyces cerevisiae ; Sprains and Strains ; Zymosan

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Syntenin Is Expressed in Human Follicular Dendritic Cells and Involved in the Activation of Focal Adhesion Kinase.

Whajung CHO ; Hyeyoung KIM ; Jeong Hyung LEE ; Seung Hee HONG ; Jongseon CHOE

Immune Network.2013;13(5):199-204. doi:10.4110/in.2013.13.5.199

Syntenin is an adaptor molecule containing 2 PDZ domains which mediate molecular interactions with diverse integral or cytoplasmic proteins. Most of the results on the biological function of syntenin were obtained from studies with malignant cells, necessitating exploration into the role of syntenin in normal cells. To understand its role in normal cells, we investigated expression and function of syntenin in human lymphoid tissue and cells in situ and in vitro. Syntenin expression was denser in the germinal center than in the extrafollicular area. Inside the germinal center, syntenin expression was obvious in follicular dendritic cells (FDCs). Flow cytometric analysis with isolated cells confirmed a weak expression of syntenin in T and B cells and a strong expression in FDCs. In FDC-like cells, HK cells, most syntenin proteins were found in the cytoplasm compared to weak expression in the nucleus. To study the function of syntenin in FDC, we examined its role in the focal adhesion of HK cells by depleting syntenin by siRNA technology. Knockdown of syntenin markedly impaired focal adhesion kinase phosphorylation in HK cells. These results suggest that syntenin may play an important role in normal physiology as well as in cancer pathology.
B-Lymphocytes ; Cytoplasm ; Dendritic Cells, Follicular* ; Focal Adhesion Protein-Tyrosine Kinases* ; Focal Adhesions* ; Germinal Center ; Humans* ; Lymphoid Tissue ; PDZ Domains ; Phosphorylation ; Proteins ; RNA, Small Interfering ; Syntenins*

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Treatment of Autoimmune Diabetes by Inhibiting the Initial Event.

Myung Shik LEE

Immune Network.2013;13(5):194-198. doi:10.4110/in.2013.13.5.194

Recent papers have shown that the initial event in the pathogenesis of autoimmune type 1 diabetes (T1D) comprises sensing of molecular patterns released from apoptotic beta-cells by innate immune receptors such as toll-like receptor (TLR). We have reported that apoptotic beta-cells undergoing secondary necrosis called 'late apoptotic' beta-cells stimulate dendritic cells (DCs) and induce diabetogenic T cell priming through TLR2. The role of other innate immune receptors such as TLR7 or TLR9 in the initiation of T1D has also been suggested. We hypothesized that TLR2 blockade could inhibit T1D at the initial step of T1D. Indeed, when a TLR2 agonist, Pam3CSK4 was administered chronically, the development of T1D in nonobese diabetic (NOD) mice was inhibited. Diabetogenic T cell priming by DCs was attenuated by chronic treatment with Pam3CSK4, indicating DC tolerance. For the treatment of established T1D, immune tolerance alone is not enough because beta-cell mass is critically reduced. We employed TLR2 tolerance in conjunction with islet transplantation, which led to reversal of newly established T1D. Dipeptidyl peptidase 4 (DPP4) inhibitors are a new class of anti-diabetic agents that have beneficial effects on beta-cells. We investigated whether a combination of DPP4 inhibition and TLR2 tolerization could reverse newly established T1D without islet transplantation. We could achieve normoglycemia by TLR2 tolerization in combination with DPP4 inhibition but not by TLR2 tolerization or DPP4 inhibition alone. beta-cell mass was significantly increased by combined treatment with TLR2 tolerization and DPP4 inhibition. These results suggest the possibility that a novel strategy of TLR tolerization will be available for the inhibition or treatment of established T1D when combined with measures increasing critically reduced beta-cell mass of T1D patients such as DPP4 inhibition or stem cell technology.
Animals ; Autoimmunity ; Dendritic Cells ; Diabetes Mellitus, Type 1* ; Dipeptidyl Peptidase 4 ; Humans ; Immune Tolerance ; Islets of Langerhans Transplantation ; Mice ; Necrosis ; Stem Cells ; Toll-Like Receptors

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Emerging Co-signaling Networks in T Cell Immune Regulation.

Keunok JUNG ; Inhak CHOI

Immune Network.2013;13(5):184-193. doi:10.4110/in.2013.13.5.184

Co-signaling molecules are surface glycoproteins that positively or negatively regulate the T cell response to antigen. Co-signaling ligands and receptors crosstalk between the surfaces of antigen-presenting cells (APCs) and T cells, and modulate the ultimate magnitude and quality of T cell receptor (TCR) signaling. In the past 10 years, the field of co-signaling research has been advanced by the understanding of underlying mechanisms of the immune modulation led by newly identified co-signaling molecules and the successful preclinical and clinical trials targeting co-inhibitory molecules called immune checkpoints in the treatment of autoimmune diseases and cancers. In this review, we briefly describe the characteristics of well-known B7 co-signaling family members regarding the expression, functions and therapeutic implications and to introduce newly identified B7 members such as B7-H5, B7-H6, and B7-H7.
Antigen-Presenting Cells ; Autoimmune Diseases ; Humans ; Ligands ; Membrane Glycoproteins ; Receptors, Antigen, T-Cell ; T-Lymphocytes

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Nanoparticle-Based Vaccine Delivery for Cancer Immunotherapy.

Yeong Min PARK ; Seung Jun LEE ; Young Seob KIM ; Moon Hee LEE ; Gil Sun CHA ; In Duk JUNG ; Tae Heung KANG ; Hee Dong HAN

Immune Network.2013;13(5):177-183. doi:10.4110/in.2013.13.5.177

Development of nano-sized carriers including nanoparticles, nanoemulsions or liposomes holds great potential for advanced delivery systems for cancer immunotherapy, as such nanostructures can be used to more effectively manipulate or deliver immunologically active components to specific target sites. Successful development of nanotechnology based platform in the field of immunotherapy will allow the application of vaccines, adjuvants and immunomodulatory drugs that improve clinical outcomes for immunological diseases. Here, we review current nanoparticle-based platforms in the efficacious delivery of vaccines in cancer immunotherapy.
Immune System Diseases ; Immunotherapy* ; Liposomes ; Nanoparticles ; Nanostructures ; Nanotechnology ; Vaccines

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