[A case of Waldenström's macroglobulinemia with cold agglutinin disease].
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Biomedical subjects
Publications and source records attributed to H Kodama.
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A monoclonal antibody, 2C12, produced against MDCC-MSB1 cells, reacted with several cell lines derived from Marek's disease (MD), including MDCC-MSB1 cells, normal chicken thrombocytes, and MD tumor cells. It did not react with cell lines derived from avian leukosis or reticuloendotheliosis, cells from normal chicken thymus and bursa, chicken kidney cells and quail fibroblast cultures inoculated with MD virus, or with erythrocytes from 1-day-old and adult chickens, cow, sheep, and horse. Anti-thrombocyte serum prepared in a rabbit reacted with thrombocytes and MDCC-MSB1 cells. The specificities of antibody 2C12 and anti-thrombocyte serum against MDCC-MSB1 cells and thrombocytes were confirmed by cross-absorption, blocking, and double-membrane fluorescent antibody tests. The existence of a polypeptide with an apparent molecular weight of 103,000, common to both MDCC-MSB1 cells and thrombocytes, was demonstrated by Western blotting analyses.
The anti-tumor activity of regional lymph node lymphocytes (RLNL) of DS mice bearing syngeneic carcinoma SC42 was observed both in intestinal cancer model and in footpad cancer model, while neither spleen cells (SPLC) nor distant lymph node lymphocytes showed any activity in Winn's tumor neutralizing test. This anti-tumor activity of RLNL was tumor specific examining between SC42 and SC115. RLNL in both cancer models did not show any cytotoxic activity against SC42 measured by 51Cr release test. However, after 9 days of culture with lectin-free T cell growth factor (LF-TCGF), the cytotoxic activity against SC42 of RLNL was induced in both cancer models. Cultured SPLC showed the cytotoxic activity against SC42 only in intestinal cancer model. Any lymphocytes from normal mice showed no cytotoxic activity against SC42 after culture with LF-TCGF. Moreover, the cytotoxic activity of cultured RLNL was tumor specific between SC42 and SC115, while that of cultured SPLC was non-specific. These results indicated that RLNL was immunologically important in tumor bearing host and the immunological significance of spleen was different between intestinal cancer and cancer of other sites.
We have developed an adoptive immunotherapy (AIT) system using syngeneic tumor-bearer-spleen cells cultured with interleukin-2 (IL-2) and soluble tumor extract. The therapeutic effect of the AIT was significantly augmented by in vivo local preadministration of a streptococcal preparation, OK-432. The previous report demonstrated a mechanism in which OK-432 augments the effect of AIT. That is, OK-432 induces IL-2 in vivo and prolongs the in vivo life span of cultured, IL-2-dependent lymphocytes (CL). This paper describes another mechanism, that is, the synergism between CL and OK-432-induced host lymphocytes. Fresh spleen cells (FSC) obtained from mice in complete remission after chemotherapy (cyclophosphamide, 100 mg/kg) showed a clear synergistic anti-tumor effect on CL, when both were injected i.p. into MOPC104E-bearing BALB/c mice which had been inoculated i.p. with 1 X 10(5) tumor cells 5 days previously. The effect was greatest when the FSC: CL ratio was 4:1, whereas the administration of either FSC or CL alone had little effect. The effector population of CL that exhibited synergism on FSC was Lyt 2+, cytotoxic T cells. FSC and CL both needed a tumor-specific combination. In addition, OK-432-induced tumor-infiltrating, intraperitoneal lymphocytes had a similar synergistic effect on CL as assessed by the transplantability of intraperitoneal cells. Probably because of this mechanism, OK-432 showed a much higher augmenting effect on AIT using CL than in vivo administration of IL-2. This therapy system using OK-432 and CL is a proper model which, through combined use of different, correlated BRMs, may bring a great effect whereas the effect of single BRM is weak.
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The phagocytosis of Vibrio anguillarum by peritoneal macrophages from normal rainbow trout was enhanced by antibody and complement. Treatment of either macrophages or the bacteria by antibody also enhanced opsonisation. Five weeks after immunisation with V anguillarum, the phagocytic activity of macrophages from rainbow trout was increased significantly compared with the activity of those from unvaccinated fish. Although agglutinin titres did not increase until three weeks after immunisation, seven out of 10 fish challenged one week after immunisation survived, indicating that immunised fish had developed resistance to vibrio infection before significant levels of antibody or phagocytic activity became detectable.
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Peripheral blood lymphocytes (PBL) from normal cattle and sheep were tested for their cytotoxic activity against several target cells using a 20-hour 51Cr release assay. The following characteristics of the effector cells were observed; 1) PBL from animals showed cytotoxic activity against two sheep cell lines (FLK and SF-28) that were transformed with bovine leukemia virus. However, normal sheep and bovine cells and Molony leukemia virus-induced mouse lymphoma cell line (YAC-1) were not killed by these cells. 2) A time course study showed that the activity was first observed at 4 to 8 hours and reached a maximum at 20 to 30 hours after incubation. 3) Cytotoxic activity was observed in both adherent and nonadherent cell fractions when PBL were passed through a nylon-wool column. This indicated that the effector cells showed some degree of adherence. 4) Treatment of PBL with carrageenan did not change the cytotoxic activity against target cells, indicating that phagocytic capability is not perhaps necessary for cytotoxicity to take place. These results indicate that the effector cells participating in the cytotoxic reaction resembled natural killer cells or natural cytotoxic cells which are present in murine and human systems. However, analysis of the cell surface markers of the effector cells is yet to be done in future studies.
The effects of prostaglandin E2(PGE2) on the degradation of collagen and non-collagenous peptides in clonal osteoblastic MC3T3-E1 cells were investigated by using highly sensitive assay methods for PZ-peptidase, collagenase-like peptidase (CL-peptidase), dipeptidyl-aminopeptidase (DAP), leucine aminopeptidase (LAP), and post-proline cleaving enzyme (PPCE). PGE2, at concentrations of 0.1 to 4.0 micrograms/ml, doubled the PZ-peptidase and CL-peptidase activities in the cells on 24 h culturing in a dose-dependent manner. PGE2, at a concentration of 2.0 micrograms/ml, enhanced the specific activities of PZ-peptidase, CL-peptidase, DAP, LAP, and PPCE for 75 h after the start of PGE2 stimulation. The time dependent changes in PZ-peptidase and CL-peptidase activities showed similar patterns, and 3- and 2-fold increases were seen after 48 h, respectively. The protein and DNA contents gradually increased after addition of PGE2. Since the PZ-peptidase and CL-peptidase, involved in degradation of collagen peptides, were significantly induced by PGE2 in comparison with LAP and PPCE, involved in the degradation of non-collagenous peptides, these results show that PGE2 specifically stimulates induction of collagen catabolizing enzymes in clonal osteoblasts.
An extracellular toxic substance was separated from the cell-free culture filtrate of Vibrio anguillarum (strain NCMB571). Two fractions (GI and GII + III) obtained by Sephadex G-200 chromatography following DEAE-cellulose chromatography were lethal to rainbow trout and mice. Material separated from the GI fraction by Sepharose 4B affinity chromatography (GI-A fraction) was lethal to these animals. By sodium dodecylsulfate polyacrylamide gel electrophoresis, the GI and GI-A fractions were found to be composed of components with molecular weights of 44K and 34K, and 44K, respectively. The 44K protein band was associated with carbohydrate. Peripheral vascular disorder was observed in fish and mice that died after inoculation with GI or GI-A fraction. The toxic substance was sensitive to potassium periodate but was resistant to trypsin and acetone. Heat inactivation of the toxic substance was almost complete at 100 C for 20 min and complete at 121 C for 20 min. The toxic activity was not associated with hemolytic or proteolytic activity. Homologous antitoxin completely neutralized the toxic activity.