concanavalin-a and Pancreatic-Diseases

In studies of immune cell defects in autoimmune diabetes mellitus, we observed that complete Freund's adjuvant (CFA) prevented the onset of diabetes when injected into 8- to 10-wk-old prediabetic nonobese diabetic (NOD) mice. The prevalence of the onset of diabetes in the CFA-injected versus uninjected NOD mice was 2 of 81 (2.5%) vs. 231 of 379 (61%) among females and 2 of 44 (4.5%) vs. 83 of 336 (25%) among males, respectively. The incidence of histologically identifiable insulitis was significantly reduced in CFA-treated prediabetic female NOD mice (18%) compared with the incidence in female age-matched controls (70%). Splenocytes or Mac-(1+)-enriched splenocytes from CFA-treated NOD mice, when cotransferred with splenocytes from diabetic mice, reduced the incidence of diabetes provoked by diabetic splenocytes in vivo. In the spleen, CFA injection induced sustained increases in cell proliferation and an associated major increase in the numbers of an immature cell type that expressed the Mac-1 surface antigen. In CFA-treated NOD mice, lymphocytes derived from the spleen failed to respond in vitro to stimulation by the mitogen concanavalin A or by anti-CD3. When cocultured, Mac-1+ cells, enriched from the splenocytes of CFA-treated mice, suppressed concanavalin A- or anti-CD3-induced proliferation of T lymphocytes derived from either the spleen or thymus of untreated NOD mice. Therefore, treatment with CFA prevents the development of diabetes, and concomitantly, insulitis while stimulating the generation of splenic suppressor cells that are capable of suppressing diabetogenic T-lymphocyte function in vivo and in vitro.

Topics: Animals; Cells, Cultured; Concanavalin A; Diabetes Mellitus, Experimental; Freund's Adjuvant; Islets of Langerhans; Lymphocyte Activation; Mice; Mice, Mutant Strains; Pancreatic Diseases; Phenotype; Prediabetic State; Spleen; T-Lymphocytes

The structural proteins of infectious pancreatic necrosis virus (IPNV) have been analyzed. Two-dimensional gel electrophoresis showed that IPNV proteins are slightly acidic with apparent pIs ranging from 5.8 to 6.6. To identify the IPNV surface-located proteins, purified virus was labelled either with fluorescein isothiocyanate (FITC) or with Na 125I. After analysis by SDS-PAGE, only the major viral protein, VP2, was labelled by either procedure. The accessibility of VP2 to these reagents suggests that this protein is externally located. In addition, using Concanavalin A conjugated with FITC and IPNV labelling with 3H-mannose, evidence is present that VP2 contains carbohydrate residues.

Topics: Animals; Capsid; Capsid Proteins; Concanavalin A; Fluorescein-5-isothiocyanate; Fluoresceins; Glycosylation; Isoelectric Point; Necrosis; Pancreatic Diseases; Salmonidae; Viral Structural Proteins; Viruses

The hypertrophic duct epithelium of the pancreas, including the pyloric gland metaplasia, mucous cell hypertrophy and ductal papillary hyperplasia were studied clinico-pathologically and histochemically to examine their precancerous character. A total of 180 surgical and autopsy specimens (90 pancreata with cancer and 90 pancreata without cancer) were analysed. The overall incidence of these three types of hypertrophic epithelium in the pancreas cancer was much higher than that in the pancreas without cancer. These hypertrophic lesions appeared most frequently in the interlobular duct. The histochemical study revealed the presence of a new type of glycoprotein in these hypertrophic duct epithelia, however, this substance was not detected in the cancer cells nor in the normal epithelium. This suggests that these hypertrophic lesions may not be the precursors of cancer but rather the coexistent lesions of pancreas cancer.

Topics: Adult; Aged; Concanavalin A; Cytoplasm; Epithelium; Glycoproteins; Glycosaminoglycans; Histocytochemistry; Horseradish Peroxidase; Humans; Hypertrophy; Middle Aged; Mucoproteins; Pancreatic Diseases; Pancreatic Ducts; Pancreatic Neoplasms; Precancerous Conditions; Staining and Labeling