B cell activated co-receptor plays important roles in linkage of innate and acquired humoral immune responses. CD21 molecule in the co-receptor complex is a receptor for C3dg and CD19 molecule enhances BCR signal transduction. CD21 also expresses on the surface of follicular dendritic cells, which mediates the long-term maintenance of antigens and is indispensable for maintaining the memory of B cells. B cell activated co-receptor also has an effect on the negative selection of B cells reactive to autoantigens.
Animals ; Antigens, CD19 ; immunology ; Autoantigens ; immunology ; B-Lymphocytes ; immunology ; Humans ; Receptors, Complement 3d ; immunology ; Receptors, Immunologic

OBJECTIVETo study the cause of low immunologic function and insufficiency of immunoglobulin synthesis in neonates by detecting CD21 expression in B lymphocytes in different age group children.

METHODSThis study consisted of three age group children: 2-26 days (n=18), 6 months-2 years (n=12) and 3-12 years (n=17). CD21 expression in B lymphocytes was detected with flow cytometry. Serum levels of immunoglobulins were measured by immunoturbidimetry.

RESULTSThe percentage and the number of B lymphocytes expressing CD21 in the neonate group were significantly lower than in the other two age groups. The neonate group also showed lower mean fluorescence intension (MFI) of CD21. The percentage and the number of B lymphocytes expressing CD21 as well as the MFI of CD21 increased significantly with the age. The serum levels of IgA and IgM in the neonate group were noticeably lower than those in the other two age groups. The serum levels of IgA and IgM also increased significantly with the age.

CONCLUSIONSLow CD21 expression in B lymphocytes may be related to low function of humoral immunity in neonates.

Adolescent ; Adult ; Age Factors ; B-Lymphocytes ; chemistry ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Receptors, Complement 3d ; blood

BACKGROUNDComplement receptor type 2 (CR2) is the receptor for C3d and C3dg and for Epstein-Barr virus. The aim of our study was to explore whether CR2 can independently mediate the activation of mitogen-activated protein kinases (MAPKs, including ERK, JNK, and p38MAPK), and to highlight the molecular mechanism of CD4+ cell deletion in AIDS.

METHODSHOS cells (HOS-CR2) and HOS-CD4 cells (HOS-CD4CR2) stably expressing CR2 were established and then identified by FACS and Western blotting. Activation and blocking tests of MAPKs were assessed by Western blot. Cell proliferation was determined using Cell Titer 96((R)) Aqueous One Solution Reagent.

RESULTSFACS results showed that the positive rates of HOS-CR2 and HOS-CD4CR2 cells were greater than 96%, and Western blot showed that the CR2 expression levels on HOS-CR2 and HOS-CD4CR2 cells were high. Activation and blocking tests of MAPKs (ERK, JNK, and p38MAPK) were carried out in HOS-CR2, HOS-CD4, and HOS-CD4CR2 cells. The activation of MAPKs in HOS-CR2 cells stimulated with PMA (100 ng/ml) and NHS (10%) was identical. The activation of MAPKs increased at 5 minutes, reached a peak at 10 minutes, and decreased to baseline within 30 minutes, all in a time-dependent manner; the activation of MAPKs was blocked by anti-CR2 McAb, PD98059 (inhibitor of ERK), and Wortmanin (inhibitor of PI-3K), respectively. In HOS-CD4 cells, MAPKs were activated by HIV-gp160. In HOS-CD4CR2 cells, MAPK activation was induced by HIV-gp160, 10% NHS, and HIV-gp160 + 10% NHS; phosphorylation of p38MAPK was dramatically induced by HIV-gp160 + NHS, and lasted for 1 hour. The cell proliferation results showed that HIV-gp160 inhibited the proliferation of HOS-CD4 and HOS-CD4CR2 cells (P < 0.01) and that NHS enhanced the effect of HIV-gp160 (P < 0.01).

CONCLUSIONSThe activation of MAPKs is independently mediated by CR2 and that anti-CR2 McAb, PD98059, and Wortmanin block the activation of MAPKs, respectively. The results of the signal transduction and cell proliferation assays of HOS-CD4CR2 cells show that CR2 plays a role in the pathogenesis of HIV infection, especially in the inhibition of CD4+ cell proliferation.

Cell Division ; Cells, Cultured ; Enzyme Activation ; Flavonoids ; pharmacology ; HIV Envelope Protein gp160 ; pharmacology ; Humans ; Mitogen-Activated Protein Kinases ; metabolism ; Receptors, Complement 3d ; physiology ; Signal Transduction

Abdominal Neoplasms ; complications ; metabolism ; pathology ; surgery ; Adult ; Dendritic Cell Sarcoma, Follicular ; complications ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Female ; Humans ; Ki-1 Antigen ; metabolism ; Leukocytosis ; complications ; metabolism ; pathology ; surgery ; Receptors, Complement 3b ; metabolism ; Receptors, Complement 3d ; metabolism ; Young Adult

OBJECTIVETo study the clinical pathological features and immunophenotype of follicular dendritic cell sarcoma (FDCS) with discussion on its diagnostic clues to improve diagnostic level.

METHODSFive cases of FDCS were analyzed by clinical, pathologic and immunohistochemistry methods.

RESULTSFive cases of FDCS were located in the cervical lymph node. Microscopically, the normal architectures were effaced by ovoid, spindle-shaped with fascicular, diffuse or whorled patterns and with rich lightly eosinophilic cytoplasm, syncytial appearance. Nuclei tend to show irregular clustering, scattered multinucleated giant cell. Nucleoli often distinct, sometimes prominent. Mitotic count variable, may show significant cellular pleomorphism. Immunohistochemical studies show that the tumor cells were positive for CD21, CD35, but negative for CD1a, CD34, CK and HMB45. Under electron microscopy, the tumor cells possessed long villus cytoplasmic processes and desmosome-like junctions, Birbeck granules were absent.

CONCLUSIONSFDCS is a rare malignant tumor and differential diagnosis includes Langerhans cell sarcoma, interdigitating dentric cell sarcoma, malignant fibrous histocytoma, melanoma, metastatic spindle cell carcinoma and others. Immunohistochemistry and electron microscopy are necessary for a correct diagnosis.

Adult ; Dendritic Cell Sarcoma, Follicular ; metabolism ; pathology ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Immunohistochemistry ; Lymph Nodes ; metabolism ; pathology ; ultrastructure ; Male ; Microscopy, Electron ; Middle Aged ; Receptors, Complement 3b ; metabolism ; Receptors, Complement 3d ; metabolism

Castleman's disease is a rare disease characterized by lymph node hyperplasia. Although Castleman's disease can occur wherever lymphoid tissue is found, it rarely appears in the abdominal cavity, and is especially rare adjacent to the liver. Here, we report a rare case of Castleman's disease in the portal area that mimicked a hepatocellular carcinoma (HCC) in a chronic hepatitis B patient. A 40 year-old woman with chronic hepatitis B presented with right upper quadrant discomfort. Computed tomography and magnetic resonance imaging results showed a 2.2 cm-sized, exophytic hypervascular mass in the portal area. HCC was suspected. However, histologic examination revealed Castleman's disease. We suggest that Castleman's disease should be included as a rare differential diagnosis of a hypervascular mass in the portal area, even in patients with chronic hepatitis B.
Adult ; Carcinoma, Hepatocellular/diagnosis ; Diagnosis, Differential ; Female ; Giant Lymph Node Hyperplasia/complications/*diagnosis/pathology ; Hepatitis B, Chronic/complications/diagnosis ; Humans ; Immunohistochemistry ; Liver Neoplasms/diagnosis ; Magnetic Resonance Imaging ; Receptors, Complement 3d/metabolism ; Tomography, X-Ray Computed

Back ; Follow-Up Studies ; Humans ; Lymphoma, Follicular ; metabolism ; pathology ; Male ; Middle Aged ; Neprilysin ; metabolism ; Proto-Oncogene Proteins c-bcl-6 ; metabolism ; Receptors, Complement 3d ; metabolism ; Skin Neoplasms ; metabolism ; pathology

We investigated the clinical and biological significance of germinal centers (GC) present in the minor salivary glands of patients with Sjogren's syndrome (SS). Minor salivary gland tissue biopsies from 93 patients with SS were used to identify GC-like structures, which were confirmed by CD21-positive follicular dendritic cell networks. Patients were compared based upon sociodemographics, glandular and extraglandular manifestations, and laboratory findings including autoantibody profiles, complement, and immunoglobulin levels; EULAR SS disease activity index (ESSDAI) and SS disease damage index (SSDDI) were also measured. GC-like structures were observed in 28 of 93 SS patients (30.1%). Mean focus scores and CRP levels were significantly higher in GC-positive patients than in GC-negative patients; GC-positive patients also exhibit a higher prevalence of rheumatoid factor and anti-SS-A/Ro antibodies compared to GC-negative patients. No differences in glandular or extra-glandular manifestations were evident between groups. In conclusion, SS patients with GC-like structures in the minor salivary glands exhibited laboratory profiles significantly different from those of their GC-negative counterparts. Long-term follow-up of these patients will be necessary to determine whether these laboratory abnormalities are predictive of clinical outcomes.
Adult ; Autoantibodies/blood ; C-Reactive Protein/analysis ; Demography ; Female ; Germinal Center/*pathology ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Receptors, Complement 3d/metabolism ; Retrospective Studies ; Salivary Glands, Minor/*pathology ; Sjogren's Syndrome/immunology/metabolism/*pathology

We investigated the clinical and biological significance of germinal centers (GC) present in the minor salivary glands of patients with Sjogren's syndrome (SS). Minor salivary gland tissue biopsies from 93 patients with SS were used to identify GC-like structures, which were confirmed by CD21-positive follicular dendritic cell networks. Patients were compared based upon sociodemographics, glandular and extraglandular manifestations, and laboratory findings including autoantibody profiles, complement, and immunoglobulin levels; EULAR SS disease activity index (ESSDAI) and SS disease damage index (SSDDI) were also measured. GC-like structures were observed in 28 of 93 SS patients (30.1%). Mean focus scores and CRP levels were significantly higher in GC-positive patients than in GC-negative patients; GC-positive patients also exhibit a higher prevalence of rheumatoid factor and anti-SS-A/Ro antibodies compared to GC-negative patients. No differences in glandular or extra-glandular manifestations were evident between groups. In conclusion, SS patients with GC-like structures in the minor salivary glands exhibited laboratory profiles significantly different from those of their GC-negative counterparts. Long-term follow-up of these patients will be necessary to determine whether these laboratory abnormalities are predictive of clinical outcomes.
Adult ; Autoantibodies/blood ; C-Reactive Protein/analysis ; Demography ; Female ; Germinal Center/*pathology ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Receptors, Complement 3d/metabolism ; Retrospective Studies ; Salivary Glands, Minor/*pathology ; Sjogren's Syndrome/immunology/metabolism/*pathology

OBJECTIVETo understand Epstein-Barr virus (EBV) infection of gastric carcinoma cells.

METHODSThe authors tested the infection of a signet ring cell line HSC-39 derived from human gastric carcinoma with Akata and P3HR-1 strains of EBV. Akata and P3HR-1 infected of EBV cell clones were isolated by a limiting dilution method.

RESULTSEBV-encoded small RNAs (EBERs) were expressed in the infected cells with each EBV strain by in situ hybridization. The EBV infected parental cells and most clones expressed EBNA1, but not EBNA2, latent membrane protein (LMP) 1 and LMP2A. Both EBV strains infected parental cells and clones presented type I latency. The uninfected HSC-39 cells were negative for CD21 expression; however, the Akata but not P3HR-1-infected clones were positive for CD21 expression at mRNA level.

CONCLUSIONThese results demonstrated that EBV infecting HSC-39 by CD21-independent pathway. This study also defined a signet ring cell line as a new target for EBV.

Carcinoma, Signet Ring Cell ; pathology ; virology ; Cell Line, Tumor ; Epstein-Barr Virus Nuclear Antigens ; analysis ; Herpesvirus 4, Human ; genetics ; physiology ; Humans ; RNA, Messenger ; RNA, Viral ; analysis ; Receptors, Complement 3d ; analysis ; genetics ; physiology ; Stomach Neoplasms ; pathology ; virology