Biomedical subjects

Yong Sung Choi

Publications and source records attributed to Yong Sung Choi.

10 recordsLinked to original sources

PubMed2006

[A case of benign schwannoma in the porta hepatis].

Schwannomas or neurilemmomas are uncommon tumors arising from schwann cells of neural sheath, which most frequently affect the extremities, trunk, head and neck area. Moreover, benign schwannoma in the porta hepatis is extremely rare. Approximately, 2 cases of benign schwannoma in the porta hepatis have been reported in the literatures. We report a case of benign schwannoma in the porta hepatis occurring in a 53-year-old woman who was asymptomatic and incidentally found to have a mass. Abdominal CT scan showed a 4.5 cm-sized low attenuating mass with septum-like enhancing solid portion at porta hepatis. Abdominal exploration revealed a yellowish, cystic and encapsulated mass attached to portal vein, common bile duct, liver and duodenal wall above the hepatoduodenal ligament. There has been no evidence of recurrence during 11 months of follow-up.

Common Bile Duct↗

PubMed2006

[Clinical features of liver abscess developed after radiofrequency ablation and transarterial chemoembolization for hepatocellular carcinoma].

BACKGROUND/AIMS: Radiofrequency ablation (RFA) and transarterial chemoembolization (TACE) have been applied for treating hepatocellular carcinoma (HCC), but procedure-related complications can be a serious problem. This study was conducted to evaluate the clinical features of HCC patients who developed liver abscess after RFA and TACE, as compared to those patients without malignancy. METHODS: In our center, from December 1999 to March 2004, 31 cases of liver abscess developed after local treatment of HCC (13/751 after RFA and 18/8417 after TAE), which correspond to 5.1% of the total cases (602) of liver abscess. We evaluated the patients' clinical features, the abscess characteristics, the bacteriology, treatment modality, hospital days and mortality, as compared to those characteristics of 263 abscess patients without malignancy. RESULTS: The time required to diagnose liver abscess was longer in the TACE group (24.8+/-16.5 days) compared to that of the other two groups (12.2+/-9.0 days in the RFA group, 9.6+/-7.5 days in the controls, P=0.001). Gas-forming liver abscess is most frequently found in the RFA groups (76.9%). There were more hospitalized days for the TACE groups than for the RFA group and the controls (34.7+/-19.8 vs. 15.2+/-9.2 vs. 18.6+/-10.9 days, respectively, P<0.001). Two patients (11%) in the TACE group died of sepsis and liver failure. CONCLUSIONS: For the patients with prolonged fever after RFA and especially after TACE for HCC, a diagnosis of liver abscess should be suspected earlier to reduce the morbidity and mortality due to liver abscess per se and also the sepsis-related decompensation of the liver.

Adult↗

PubMed2005

BAFF supports human B cell differentiation in the lymphoid follicles through distinct receptors.

B cell-activating factor of the tumor necrosis factor family (BAFF/BLys) plays a critical role in B cell survival and immune responses through its three receptors: BAFF receptor (BAFF-R/BR3), transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI) and B cell maturation antigen (BCMA). Using specific antibodies, we have investigated the expression of BAFF-R on human tonsillar B cells and their functional roles in naive and germinal center (GC) B cell differentiation. Our studies show that BAFF-R is the dominant receptor on naive B cells. However, three receptors are differentially modulated during in vitro GC-B cell differentiation. BAFF-R expression increased initially and then decreased with a corresponding induction of TACI and BCMA expression during differentiation to plasma cells (PCs). Consistently, blocking of BAFF-R alone with specific mAb inhibited GC-B cell proliferation and PC generation in the early period of their differentiation, whereas depletion of BAFF with TACI-Ig exhibited consistent inhibition throughout the differentiation. Finally, histological and molecular analyses of human tonsil tissue revealed that follicular dendritic cells produce BAFF. In conclusion, BAFF in the GC plays an important role through more than one receptor, and the three known receptors are differentially modulated as GC-B cells differentiate to PCs.

Antibodies, Monoclonal↗

PubMed2005

How do follicular dendritic cells interact intimately with B cells in the germinal centre?

The germinal centre is a dynamic microenvironment where antigen-activated B cells rapidly expand and differentiate, generating plasma cells and memory B cells. These cellular events are accompanied by dramatic changes in the antibody molecules that undergo somatic hypermutation and isotype switching. Follicular dendritic cells (FDCs) are the stromal cells located in the germinal centre. Although the capacity of FDCs to present antigen to B cells through antigen-antibody complexes has been recognized for many years, additional critical functions of FDCs have only recently been recognized. FDCs prevent apoptosis of germinal centre B cells and stimulate cellular interaction and proliferation. Here, we review the FDC signalling molecules that have recently been identified, some of which offer potential therapeutic targets for autoimmune diseases and B-cell lymphomas.

B-Lymphocytes↗

PubMed2004

Follicular dendritic cells produce IL-15 that enhances germinal center B cell proliferation in membrane-bound form.

Factors that control the survival and proliferation of Ag-stimulated B cells within the germinal center (GC) are crucial for humoral immune responses with high affinity Abs against infectious agents. The follicular dendritic cell (FDC) is known as a key cellular component of the GC microenvironment for GC-B cell survival and proliferation. In this study, we report that IL-15 is produced by human FDC in vivo and by an FDC cell line, FDC/HK cells, in vitro. IL-15 is captured by IL-15Ralpha on the surface of FDC/HK cells. The surface IL-15 is functionally active and augments GC-B cell proliferation. Because GC-B cells have the signal-transducing components (IL-2/15Rbetagamma), but not a receptor for binding of soluble IL-15 (IL-15Ralpha), IL-15 signaling is possibly transduced by transpresentation from FDCs to GC-B cells via cell-cell contact. Together, these results suggest that IL-15 from FDC, in membrane-bound form, plays an important role in supporting GC-B cell proliferation, proposing a new target for immune modulation as well as treatment of B cell tumors of GC origin.

Adjuvants, Immunologic↗

PubMed2004

Novel follicular dendritic cell molecule, 8D6, collaborates with CD44 in supporting lymphomagenesis by a Burkitt lymphoma cell line, L3055.

The lymphoid follicle is a specialized microenvironment for the differentiation of antigen (Ag)-activated B cells; the major stromal cell components in lymphoid follicle are the follicular dendritic cells (FDCs). At the same time, most of the B-cell lymphomas originate from the germinal center, and the generation and blast transformation of B-cell lymphoma occurs in close association with FDCs in the early stage of tumorigenesis. To study the functional roles of FDCs in lymphomagenesis, we established an inducible tumor model. The human B-cell lymphoma cell line, L3055, formed solid tumors only when inoculated with an FDC line, HK. In addition, 2 FDC-signaling molecules (FDC-SMs), a novel protein 8D6 and 4G10/CD44, are required for tumor formation in vivo, because monoclonal antibodies (mAbs) specific to these 2 proteins inhibited lymphomagenesis completely when they were inoculated with L3055 and HK cells. However, these 2 FDC-SMs have distinct functional roles in tumor formation. FDC-SM-8D6 enhances L3055 cell proliferation, whereas FDC-SM-4G10/CD44 inhibits its apoptosis. Identification of the functional roles of these critical FDC-SMs may lead to the discovery of therapeutic drugs that suppress the survival and growth of lymphoma cells.

3T3 Cells↗

PubMed2003

A workshop on the marrow microenvironment and hematological malignancy.

The Division of Cancer Biology of the National Cancer Institute hosted a workshop on hematological malignancies and the marrow microenvironment in Rockville, Maryland in the fall of 2002. There were 22 invited participants from the United States, Canada, and Europe, and the workshop was organized into disease-specific sessions. The sessions were designed to explore the basic science and therapeutic applications related to the stromal and nonstromal components of the marrow in malignant hematological diseases.

Animals↗

PubMed2002

Distinct response of human B cell subpopulations in recognition of an innate immune signal, CpG DNA.

Innate immunity has recently gained renewed interest in its ability to regulate adaptive immunity. Among the innate immune signals, CpG DNA has revealed its potential as a vaccine adjuvant. However, the cellular mechanism for the effect of CpG DNA on the humoral immune response is not well understood. Here, we investigated the effects of CpG DNA on human B cell differentiation using highly purified B cell subsets: naive, germinal center (GC), and memory B cells. In the in vitro culture system that mimics the primary or secondary immune response in vivo, CpG DNA markedly augmented the proliferation and generation of plasma cells from naive and memory B cells. CpG DNA dramatically increased plasma cell generation from GC B cells. However, CpG DNA did not have effect on memory B cell generation from GC B cells. These results suggest that CpG DNA potentiates the B cell adaptive immune response by enhancing terminal differentiation, but does not affect the generation of memory B cells.

Adjuvants, Immunologic↗

PubMed2002

Protection of CLL B cells by a follicular dendritic cell line is dependent on induction of Mcl-1.

Chronic lymphocytic leukemia (CLL) B cells have defects in apoptosis pathways and therefore accumulate in vivo. However, when removed from the patient and cultured in vitro, these malignant cells rapidly undergo apoptosis. Recent studies suggest that leukemia cell survival is influenced by interactions with nonleukemia cells in the microenvironment of lymph nodes, marrow, and other tissues. To model such cell-cell interactions in vitro, we cultured freshly isolated CLL B cells with a follicular dendritic cell line, HK. CLL B cells cocultured with HK cells were protected from apoptosis, either spontaneous or induced by treatment with anticancer drugs. Protection against spontaneous apoptosis could also be induced by coculturing the CLL B cells with normal dendritic cells (DCs) or with a CD40-ligand (CD154)-expressing fibroblast cell line. Examination of the expression of several apoptosis-regulatory proteins revealed that coculture with HK cells or DCs induced up-regulation of the antiapoptotic Bcl-2 family protein Mcl-1 in CLL B cells, whereas CD40 ligation increased expression of Bcl-X(L). Cell-cell contact was required for HK-induced protection, and introducing neutralizing antibodies against various adhesion molecules showed that CD44 was involved in HK-mediated survival, whereas CD40, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were not. Anti-CD44 antibodies also blocked Mcl-1 induction by HK cells. Mcl-1 antisense oligonucleotides reduced leukemia cell expression of Mcl-1, and significantly suppressed HK-induced protection against apoptosis, whereas control oligonucleotides had no effect. Thus, HK cells protect CLL B cells against apoptosis, at least in part through a CD44-dependent mechanism involving up-regulation of Mcl-1, and this mechanism is distinct from that achieved by CD40 ligation. Consequently, the particular antiapoptotic proteins important for CLL survival may vary depending on the microenvironment.

Apoptosis↗

PubMed2002

Follicular dendritic cell-signaling molecules required for proliferation and differentiation of GC-B cells.

To study the functional role of follicular dendritic cells (FDC) in germinal center (GC)-B cell differentiation, we have established an in vitro experimental model that mimics GC-reactions in vivo. Using this culture system, we have characterized the distinct function of FDC from activated T cells. The primary function of FDC is to prevent apoptosis and support proliferation of GC-B cells, whereas activated T cells induce the differentiation of GC-B cells by providing CD40L and cytokines. Furthermore, we have identified two FDC-signaling molecules that mediate proliferation of GC-B cells in vitro and in vivo.

Animals↗