ABSTRACT
Rabbit antisera were obtained against cytotoxic small peritoneal lymphocytes (IPEL) of CBA (H-2k) mice immune to alloantigens C57BL/6 (H-2b) and to the enriched 5-day MLC cytotoxic blast lymphocytes (MLC--CL). After appropriate absorption by cells and tissues of intact mice the cytotoxicity of the sera was lost relative to normal lymphoid cells. The absorbed anti-CPL serum inhibited, in the presence of complement, the cytotoxic effect of CPL but not that of MLC--CL on 51Cr-labeled allogeneic macrophages. This inhibition was restricted by idiotypic and strain specificity. Conversely, the absorbed anti-MLC--CL serum inhibited the cytotoxic effect of both CPL and MLC--CL of various mouse strains, irrespective of their immunologic specificity. It is supposed that the effect of the anti-CPL serum is mainly caused by antibodies againts idiotypic determinants of the killer T receptors, whereas the effect of the anti-MLC--CL serum is due to antibodies against differentiation antigens of the proliferating lymphocytes.
Subject(s)
Antigens, Surface/immunology , Epitopes , H-2 Antigens/immunology , Immune Sera/pharmacology , Killer Cells, Natural/immunology , Animals , Antibody-Dependent Cell Cytotoxicity , Carcinoma, Ehrlich Tumor/immunology , Lymphoma/immunology , Mice , Mice, Inbred AKR/immunology , Mice, Inbred BALB C/immunology , Mice, Inbred C57BL , Mice, Inbred CBA/immunology , Species SpecificityABSTRACT
Investigations were carried out on male CBA mice with casein-induced amyloidosis. Fragments of spleens from the amyloid and intact donors were transplanted simultaneously to the opposite kidney poles, subcapsularly, to the intact and amyloid recipients. Amyloid deposits were found in 40 per cent of intact recipients both in their own spleens and in the grafts from intact donors. In amyloid recipients amyloid deposits developed in the grafts from intact donors only in 5 per cent of the animals (observation periods from 5 days to 6 months after the transplantation). It is amyloidogenic cells migration and the depression of this mechanism in amyloid mice.
Subject(s)
Amyloidosis/transmission , Spleen/transplantation , Amyloidosis/etiology , Amyloidosis/pathology , Animals , Male , Mice , Mice, Inbred CBA , Spleen/pathology , Transplantation, HomologousABSTRACT
Induction of murine amyloidosis by contact sensitization with hapten--dinitrochlorobenzene is described. Three to five applications of 15--25% dinitrochlorobenzene solution in acetone during two weeks are necessary for this. Within 3 weeks after the 1st application amyloidosis develops involving consecutively the spleen, liver, kidney and heart. Such consequence of the organ involvement and tinctorial pecularities are typical of murine amyloidosis.
Subject(s)
Amyloidosis/chemically induced , Dinitrochlorobenzene/immunology , Disease Models, Animal , Nitrobenzenes/immunology , Amyloidosis/immunology , Animals , Dinitrochlorobenzene/administration & dosage , Immunization , Mice , Time FactorsABSTRACT
Contact dermatitis was induced in BALB/c mice by means of cutaneous application of dinitrochlorbenzol (DNCB) solution. Peritoneal macrophages from DNCB-sensitized and intact mice were cultivated in flat tubes for 48 hours after the 20th day of the experiment, when the DNCB cutaneous test became positive. A suspension of the peripheral lymph node lymphocytes was added to this culture. The lymphocytes fromthe DNCB-sensitized mice had a cytotoxic effect (CTE) on the target cells (peritoneal macrophages) during the co-incubation; the STE was tested with trypane blue in 48 hours. No macrophage lysis was observed in combined incubation of cells from the intact mice.
Subject(s)
Dermatitis, Contact/immunology , Dinitrochlorobenzene , Lymphocytes/immunology , Macrophages/immunology , Nitrobenzenes , Animals , Cytotoxicity Tests, Immunologic , Male , Mice , Mice, Inbred BALB CABSTRACT
In experiment on 33 mice, line C57Bl, the effect of changed vascular-tissue permeability following administration of histamine and anti-histamine preparation diprazin (pipolphen) on the development of amyloidosis was studied. It was shown that histamine stimulated the development of amyloidosis in mice, causing besides generalized vascular disorders and a pronounced mast-cell reaction with degranulation of these cells, whereas diprazin, on the contrary, inhibited amyloidogenesis in mice. Differences between experimental and control groups were identified using the morphometric method and were confirmed statistically. The difference in the degree of amyloidosis revealed against the background of administration of histamine and diprazin testified to a certain extent to the role of impaired vascular-tissue permeability in the pathogenesis of amyloidosis.