IL-17 is produced by RAR-related orphan receptor gamma t (RORγt)-expressing cells including Th17 cells, subsets of γδT cells and innate lymphoid cells (ILCs). The biological significance of IL-17-producing cells is well-studied in contexts of inflammation, autoimmunity and host defense against infection. While most of available studies in tumor immunity mainly focused on the role of T-bet-expressing cells, including cytotoxic CD8+ T cells and NK cells, and their exhaustion status, the role of IL-17-producing cells remains poorly understood. While IL-17-producing T-cells were shown to be anti-tumorigenic in adoptive T-cell therapy settings, mice deficient in type 17 genes suggest a protumorigenic potential of IL-17-producing cells. This review discusses the features of IL-17-producing cells, of both lymphocytic and myeloid origins, as well as their suggested pro- and/or anti-tumorigenic functions in an organ-dependent context. Potential therapeutic approaches targeting these cells in the tumor microenvironment will also be discussed.
The regional distribution and relative frequency of some endocrine cells in the pancreas of the Korean aucha perch, Coreoperca herzi Herzenstein belonging to the family Serranidae in order Perciformis, were observed using specific mammalian antisera against serotonin, insulin, glucagon, somatostatin and human pancreatic polypeptide (hPP) by peroxidase antiperoxidase (PAP) method. The pancreas was divided into four portions (principal and secondary islets, exocrine and pancreatic duct regions). In addition, the pancreatic islet regions were further subdivided into three regions (central, mantle and peripheral regions). Spherical to spindle or occasionally round to oval immunoreactive (IR) cells were demonstrated in the pancreatic islets and exoccrine portions, but no cells were detected in the pancreatic duct portions. In the principal islets, serotonin-IR cells were not detected but most of insulin-IR cells were located in the central regions and they were also demonstrated in the mantle and peripheral regions in moderate and rare frequencies, respectively. Glucagon- and hPP-IR cells were mainly situated in the mantle regions but the cells were also demonstrated in the peripheral regions in relatively lower frequency. Somatostatin-IR cells were evenly distributed in the central and mantle regions in a few frequency and cells were also demonstrated in the peripheral regions in rare frequency. Cell clusters were consisted of hPP-IR cells that were situated in the peripheral to mantle regions. In the secondary islet portions, serotonin-IR cells were randomly distributed throughout the whole pancreatic islet regions but lower frequency was detected in the peripheral regions compared to that in central and mantle regions where cells were detected in a few frequency, respectively. Insulin-IR cells were restricted to the central regions in numerous frequency and glucagon-IR cells were evenly distributed in the mantle and peripheral regions in moderate frequencies, respectively. Somatostatin-IR cells were observed in the central and mantle regions in moderate and a few frequencies, respectively. In addition, hPP-IR cells showed similar distributional patterns to those of glucagon-IR cells except cells were also located in the central regions in rare frequency. In the exocrine portions, only glucagon- and hPP-IR cells were demonstrated in rare and a few frequencies, respectively. In conclusion, the regional distribution and relative frequency of pancreatic endocrine cells of the Korean aucha perch showed general patterns, which were observed in other teleost. However, some species-dependent different distributional patterns and/or relative frequencies were also demonstrated especially to serotonin-IR cells. In pancreas of the Korean aucha perch, insulin-IR cells were the most predominant cell type followed by glucagon-, somatostatin-, hPP- and serotonin-IR cells.
This study was attempted to comparative investigate the types and regional distribution of the endocrine cells in several vertebrates immunohistochemically using seven antisera. From carp pancreas could be observed 4 types which are insulin-, glucagon-, som- and BPP-immunoreactive cells. Insulin-immunoreactive cells were mainly distributed at the periphery and a few cells occupied the central region of the islets. Glucagon-immunoreactive cells were distributed at the periphery of the islets, and som - and BPP-immunoreactive cells were located at the central region. From frog pancreas could be observed 4 types which are insulin-, glucagon-, som- and BPP-immunoreactive cells. Insulin-immunoreactive cells were distributed throughout the islets. Som-immunoreactive cells were distributed at the periphery of the islets, and glucagon- and BPP-immunoreactive cells were found as single cell or as small groups located between the pancreatic acini. From snake pancreas could be observed 3 types which are insulin-, glucagon- and som -immunoreactive cells. Insulin-immunoreactive cells were distributed throughout the small islets, and they also were scattered at the periphery of the large islets. Glucagon-immunoreactive cells were distributed at the periphery of the islets, whereas som-immunoreactive cells were occupied the central region. From Ogolgae pancreas could be observed 4 types which are insulin-, glucagon-, som-and BPP-immunoreactive cells. Insulin-immunoreactive cells were distributed throughout the small islets, but at the periphery of the large one. Glucagon- immunoreactive cells were distributed at the periphery of the small islets and in the large islets showed scattering entired. Som-immunoreactive cells were distributed at the periphery of the small islets and in the large islets were located at the central region. A small numbers of BPP-immunoreactive cells were located at the periphery of the small islets and the exocrine regions. From the pancreas of the Korean native goat could be observed 6 types which are insulin-, glucagon-, som-, BPP-, 5-HT- and porcine-CG-immunoreactive cells. Insulin-immunoreactive cells were distributed throughout the islets. Som-immunoreactive cells were located at the periphery of the islets, but a tew were scattered at the central region of islets and in the epithelium of the secretory duct. Glucagon-, BPP-, 5-HT- and porcine CG-immunoreactive cells were distributed at the periphery of the islets. These findings indicated that the regional distribution patterns and cell types of pancreatic endocrine cells in vertebrates varies considerably among phylogenetically different vertebrates.
Embryonic stem (ES) cells have property of self-renewal and can differentiate into the cells of all three primary germ layers. Recently, many growth factors, alteration of culture condition and gene modifications have been used to differentiate mouse and human ES cells into specific cell types. This study was performed to evaluate the differentiation protocol for human ES cells to the endodermal lineage cells. Human ES cells (Miz-hESl ) were cultured on STO feeder layer mitotically inactivated with mitemycin C, and embryoid bodies (EBs) were formed by suspension culture. Differentiation protocol of EBs consisted of three steps: stage I, culture of EBs for 6 days with ITSFn medium; stage II, culture of stage I cells for 8 days with N2 medium ; stage III, culture of stage II cells for 22 days with N2 medium. mRNA levels of the endodermal lineage differentiation genes were analyzed by semi- quantitative RT-PCR. The Oct-4 expression, a marker of the pluripotent state, was detected in undifferentiated human ES cells but progressively decreased after EBs formation. Differentiating human ES cells expressed marker genes of endodermal differentiation and pancreatic islet cells. GATA4, a-fetoprotein, Glut-2, and Ngn3 were expressed in all stages. However, albumin and insulin were expressed in only stage III cells. The human ES cells can be differentiated into endodermal lineage cells by multiple step culture system using various supplements. We are developing the more effective protocols for guided differentiation of human ES cells.
Kim, Min Ki;Lee, Ara;Hwang, Yu Kyeong;Kang, Chang-Yuil;Ha, Sang-Jun
IMMUNE NETWORK
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제14권4호
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pp.207-218
/
2014
Chronic virus infection leads to the functional impairment of dendritic cells (DCs) as well as T cells, limiting the clinical usefulness of DC-based therapeutic vaccine against chronic virus infection. Meanwhile, B cells have been known to maintain the ability to differentiate plasma cells producing antibodies even during chronic virus infection. Previously, ${\alpha}$-galactosylceramide (${\alpha}GC$) and cognate peptide-loaded B cells were comparable to DCs in priming peptide-specific $CD8^+$ T cells as antigen presenting cells (APCs). Here, we investigated whether B cells activated by ${\alpha}GC$ can improve virus-specific T cell immune responses instead of DCs during chronic virus infection. We found that comparable to B cells isolated from naïve mice, chronic B cells isolated from chronically infected mice with lymphocytic choriomeningitis virus (LCMV) clone 13 (CL13) after ${\alpha}GC$-loading could activate CD1d-restricted invariant natural killer T (iNKT) cells to produce effector cytokines and upregulate co-stimulatory molecules in both naïve and chronically infected mice. Similar to naïve B cells, chronic B cells efficiently primed LCMV glycoprotein (GP) 33-41-specific P14 $CD8^+$ T cells in vivo, thereby allowing the proliferation of functional $CD8^+$ T cells. Importantly, when ${\alpha}GC$ and cognate epitope-loaded chronic B cells were transferred into chronically infected mice, the mice showed a significant increase in the population of epitope-specific $CD8^+$ T cells and the accelerated control of viremia. Therefore, our studies demonstrate that reciprocal activation between ${\alpha}GC$-loaded chronic B cells and iNKT cells can strengthen virus-specific T cell immune responses, providing an effective regimen of autologous B cell-based therapeutic vaccine to treat chronic virus infection.
This study was carried out to examine the role of small cells and oval cells in cholangiocarcinogenesis in the hamsters infected with Clonorchis(C) sinensis. Forty two female Syrian golden hamsters were divided into two groups. Group I was for the induction of the cholangiocarcinoma, which was infected orally with C sinensis and given dimethylnitrosamine(15ppm) in drinking water for 4 weeks. Group II was served as control. More than 5 heads of hamsters in each group were sacrificed at 4, 7, 11 and 15 weeks after the beginning of the experiment. The livers were examined histopathologically, electron microscopically and immunohistochemically. The results obtained were as follows; 1. Cholangiocarcinomas were occurred in 1 of 6 animals at 11 weeks and in 4 of 6 animals at 15weeks after the beginning of the experiment. 2. Small cells and oval cells were proliferated around the portal triads from 4 weeks and peaked at 11 weeks, and slightly decreased after then. 3. The strong positive reaction to the $\alpha$-fetoprotein was shown in many of small cells and oval cells. But ductlike oval cells, which were arranged rosette form, showed week positive reaction to the $\alpha$-fetoprotein. 4. Most of small cells and oval cells showed negative reaction to the cytokeratin. But weak positive reaction in ductlike oval cells, and moderate positive reaction in cholangiocarcinoma cells were observed. These results suggested that cholangiocarcinoma induced by infection of C sinensis was believed to originate from the proliferated small cells around the portal triads which would be able to differentiate to the oval cells, ductlike oval cells, and cholangiocarcinoma cells gradually.
This study investigated whether a correlation exists between environmental physical and biochemical factors and adherence of Candida albicans to human buccal epithelial cells by using normal and UV-irradiated strains. The results were as follows: 1. The percentage of germ tube forming activities of normal Candida albicans was 91.5% and UV-irradiated Candida albicans was 15.0%. The $LD_{50}$ of normal strains in mice were $1.0{\times}10\;cells/ml$, but could not be observed in the UV-irradiated strains even with $1.0{\times}10\;cells/ml$. It demonstrated that the virulence is decreased in the UV-irradiated strain. 2. The adherence of normal Candida albicans to human buccal epithelial cells($166{\pm}29{\sim}207{\pm}17\;cells$/100 epithelial cells) was significantly greater than UV-irradiated Candida albicans($99{\pm}21{\sim}131{\pm}25\;cells$/100 epithelial cells). 3. Candida albicans cultured at $37^{\circ}C$ adhered to buccal epithelial cells($166{\pm}16{\sim}207{\pm}17\;cells$/100 epithelial cells) in greater numbers than cultured at $25^{\circ}C$($80{\pm}15{\sim}143{\pm}22\;cells$/100 epithelial cells). 4. On comparison of the adherence of viable and nonviable(heat-killed) Candida albicans to human buccal epithelial cells, the nonviable Candida albicans demonstrated poorer adherence than viable Candida albicans. 5. Adherence in vitro of Candida albicans to human epithelial cells appeared to be effected by the pH. The adherence ability was maximum increased at pH 7.0($187{\pm}22\;cells$/100 epithelial cells) other than experimental pH. 6. The adherence was proportional to the incubation time and the Candida cell concentration in the suspension. 7. A strong correlation was shown between germ tube forming activity and increased adherence of Candida albicans to human epithelial cells, indicating that germ tube forming activity were responsible for candidal virulence.
Boo, Sun-Jin;Piao, Mei Jing;Kang, Kyoung Ah;Zhen, Ao Xuan;Fernando, Pincha Devage Sameera Madushan;Herath, Herath Mudiyanselage Udari Lakmini;Lee, Seung Joo;Song, Seung Eun;Hyun, Jin Won
Biomolecules & Therapeutics
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제30권5호
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pp.447-454
/
2022
Few studies have evaluated the role of autophagy in the development of oxaliplatin (OXT) resistance in colon cancer cells. In this study, we compared the role of autophagy between SNU-C5 colon cancer cells and OXT-resistant SNU-C5 (SNU-C5/OXTR) cells. At the same concentration of OXT, the cytotoxicity of OXT or apoptosis was significantly reduced in SNU-C5/OXTR cells compared with that in SNU-C5 cells. Compared with SNU-C5 cells, SNU-C5/OXTR cells exhibited low levels of autophagy. The expression level of important autophagy proteins, such as autophagy-related protein 5 (Atg5), beclin-1, Atg7, microtubule-associated proteins 1A/1B light chain 3B I (LC3-I), and LC3-II, was significantly lower in SNU-C5/OXTR cells than that in SNU-C5 cells. The expression level of the autophagy-essential protein p62 was also lower in SNU-C5/OXTR cells than in SNU-C5 cells. In SNU-C5/OXTR cells, the production of intracellular reactive oxygen species (ROS) was significantly higher than that in SNU-C5 cells, and treatment with the ROS scavenger N-acetylcysteine restored the reduced autophagy levels. Furthermore, the expression of antioxidant-related nuclear factor erythroid 2-related factor 2 transcription factor, heme oxygenase-1, and Cu/Zn superoxide dismutase were also significantly increased in SNU-C5/OXTR cells. These findings suggest that autophagy is significantly reduced in SNU-C5/OXTR cells compared with SNU-C5 cells, which may be related to the production of ROS in OXT-resistant cells.
Many cell types are known to stimulate $CD8^+$ T cells in allogeneic recognition such as mixed lymphocyte reaction (MLR). Whereas dendritic cells are most potent among them. T cells are usually considered very poor in stimulating $CD8^+$ T cells although there are some tumor cells that are weakly stimulatory. T cells, as a stimulator, cultured in the presence of concanavalin A that were otherwise nonstimulatory to $CD8^+$ T cells appeared to stimulate $CD8^+$ T cells strongly when they were pretreated with neuraminidase. The enhancement of MLR by neuraminidase could be achieved by treating either the stimulators or responders with neuraminidase. Removal of negatively-charged sialic acid moieties from the cell surface, which reduced electrostatic repulsion between responders and stimulators to give better cell-cell contact might be responsible for the enhanced MLR. In addition, neuraminidase treatment also appeared to deliver activation signal to responding T cells since it could activate $CD8^+$ T cells in synergy with phorbol myristate acetate. The maximal responses were observed when both responders and stimulators were treated with neuraminidase.
The receptor activator of NF-${\kappa}B$ ligand (RANKL), a member of the tumor necrosis factor ligand family, has extensive functions beyond osteoclast development. RANKL is expressed in many immune cells such as osteoblasts, osteocytes, marrow stromal cells, activated T cells, synovial cells, keratinocytes, and mammary gland epithelial cells as well as in various tissues. The ligation of RANK by RANKL promotes dendritic cells (DCs) survival through prosurvival signals and the up-regulation of the anti-apoptotic proteins Bcl-2 and Bcl-$x_L$ and plays a crucial role in DCs-mediated Th1 differentiation. Therefore, RANKL plays an important role in the regulation of DCs/T cells-mediated specific immunity. This review will briefly inform our current understanding of the role of RANKL signaling in T cells-DCs communication in the immune system.
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