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Biomedical subjects

R C Mellors

Publications and source records attributed to R C Mellors.

At least 37 records · Page 2Linked to original sources
PubMed1971

Wild-type Gross leukemia virus and the pathogenesis of the glomerulonephritis of New Zealand mice.

The pathogenesis of the spontaneous glomerulonephritis of NZB and (NZB x NZW) F(1) hybrid mice is related at least in part to the formation of natural antibody against antigens of the G (Gross) system, and apparently to the deposition in the glomeruli of immune complexes of G natural antibody with G soluble antigen (GSA), type-specific antigen specified by wild-type Gross leukemia virus. G natural antibody and GSA are detectable in the acid-buffer eluate of the kidneys of NZB mice during the course of the glomerulonephritis. (NZB x NZW) F(1) hybrid mice develop glomerulonephritis and produce GSA and free G natural antibody earlier in life than do NZB mice. The proteinuria manifestation of the gomerulonephritis of (NZB x NZW) F(1) hybrid mice becomes increasingly prevalent as GSA undergoes immune elimination from the circulation. Gross leukemia virus-specified antigens together with bound immunoglobulins are located in the glomerular lesions of (NZB x NZW) F(1) hybrid mice, both in the mesangium as observed in NZB mice and also in the wall of the peripheral capillary loops of the glomeruli.

AKR murine leukemia virus↗
PubMed1971

Natural thymocytotoxic autoantibody and reactive antigen in New Zealand black and other mice.

Naturally occurring thymocytotoxic autoantibody (NTA) was detected by cytotoxic test in the sera of very young New Zealand Black mice (within 1 month after birth); the incidence was 100% at 3 months of age. Some mice from other strains also had NTA, but at an older age and with lower incidence and antibody titer. NTA had optimal activity at 4 degrees C but was also strongly reactive at 37 degrees C. It was cytotoxic for thymocytes of all strains of mice tested. Whereas only thymocytes were highly sensitive to NTA, the reactive antigen was demonstrated by absorption test in the thymus, lymph node, spleen, and brain of adult mice. It could be demonstrated only in the thymus of newborn mice.The distribution of NTA-reactive antigen suggests the presence of an antigen distinct from any so far described on the cell surface of mouse thymocytes. Gel filtration of NZB mouse serum suggests that NTA is an IgM. Mouse thymocytes sensitized with NTA in vitro became highly susceptible to phagocytosis by syngeneic macrophages.

Age Factors↗
PubMed1969

Further implication of murine leukemia-like virs in the disorders of NZB mice.

Further evidence implicating murine leukemia-like virus in the disorders of NZB mice was afforded by a study of antigens associated with murine leukemia virus (MuLV). MuLV group antigens were prevalent in extracts of spleen, kidney, and, to a lesser extent, thymus throughout a substantial portion of the life span of NZB mice as well as in extracts of lymphomas and sarcomas indigenous to the strain. G (Gross) soluble antigen, type-specific antigen, was first detected in plasma of untreated NZB mice at 3 months of age. G soluble antigen production increased thereafter in line with age, with 50% of reactions becoming positive at 5.3 months and 100% at 7 to 9 months. From months 3 to 9, the time-response curve for positive conversion of direct antiglobulin (Coombs) tests in untreated NZB mice corresponded closely to that for G soluble antigen production. Beyond the 9th month, G soluble antigen underwent elimination from the plasma of NZB mice, with positive reactions reduced to 50% at 13.3 months and to 0% at 18 months. G natural antibody was first detected in the serum of NZB mice at about 10 months of age and increased thereafter in line with age. The curves for G antibody production and G soluble antigen elimination bore a reciprocal relation to each other with crossover at 50% response occurring at 13.3 months. Significant proteinuria, a functional manifestation of membranous glomerulonephritis, became increasingly prevalent in female NZB mice as G soluble antigen was eliminated from plasma. Cumulative mortality of female NZB mice, mainly attributable to renal glomerular disease, increased in phase with G antibody production. MuLV group antigens were identified in the glomerular lesions by the immunofluorescence method. Positive conversion of direct antiglobulin tests was significantly delayed by vaccinating baby NZB mice with formaldehyde-inactivated cell-free filtrates of older NZB mouse spleens. The plasmas of vaccinated NZB mice with negative direct antiglobulin reactions at 4 to 7 months were likewise negative when tested for G soluble antigen. The 50% response time for G antibody production in the vaccinated NZB mice occurred at 7.3 months, that is, 6 months earlier than in untreated NZB mice. The collective findings implicate murine leukemia-like virus in the etiology of autoimmune hemolytic disease and membranous glomerulonephritis, as well as malignant lymphoma, of NZB mice and suggest that virus-specified cell-surface and soluble antigen is a factor in the immunopathogenesis of the renal disease and possibly also the autoimmune hemolytic disease.

Animals↗
PubMed1967

Immunopathology of NZB/BL mice. VI. Virus separable from spleen and pathogenic for Swiss mice.

Hemolytic disease characterized by slight anemia, reticulocytosis, hemosiderosis, extramedullary hematopoiesis, and positive indirect antiglobulin (Coombs') tests and renal disease with proteinuria, hypoalbuminemia, and glomerular lesions were produced in Swiss mice by neonatal intraperitoneal inoculation of cell-free filtrates prepared from the spleens of old NZB/Bl mice. Lymphoid cell and plasma cell hyperplasia as well as hypergammaglobulinemia occurred in some of these inoculated mice. Type "C" murine oncogenic virus-like particles, indistinguishable from those previously described (1), were shown by electron microscopic study to be present in distinctive locations, notably in the basal foldings of convoluted tubules in the kidneys of a newborn NZB/Bl mouse, old NZB/Bl mice, a CBA x NZB F(1) hybrid mouse, and a Swiss mouse inoculated with NZB/Bl spleen cell-free filtrate. These observations point to two (perhaps related) circumstances which may be requisites for the pathogenic action of this newly discovered virus within and outside the strain NZB: infection of newborn, or infant, mice; persistent, possibly tolerant, infection of adult mice.

Anemia, Hemolytic↗
PubMed1966

Immunopathology of NZB/BL mice. V. Viruslike (filtrable) agent separable from lymphoma cells and identifiable by electron microscopy.

A filtrable agent separable from transplantable malignant lymphomas of NZB/Bl mice was capable, upon inoculation into preweanling NZB/Bl mice, of inducing lymphoid cell hyperplasia, hypergammaglobulinemia, proteinuria, hypoalbuminemia, and pathological changes (focal membranous glomerulonephritis) of kidneys-renal functional and structural changes qualitatively similar to those of spontaneous occurrence in older NZB/Bl mice. Viruslike particles with close resemblance to the typical "C" type murine oncogenic virus particles were identified by means of electron microscopy in NZB/Bl mouse tissues and cells, including malignant lymphoma cells, benign lymphoid cells of thymus and spleen, epithelial cells of renal tubules, and extracellular sites. The relevance of these observations, the first of their kind dealing with NZB/Bl mice, is discussed in relation to the several immunopathological disorders which characterize this strain of mice.

Animals↗
PubMed1966

Autoimmune disease in NZB/BL mice. 3. Induction of membranous glomerulonephritis in young mice by the transplantation of spleen cells from old mice.

The transplantation of spleen cells from old NZB/Bl mice with renal disease induced both the structural and the functional changes of membranous glomerulonephritis in young NZB/Bl mice within a few weeks and well in advance of its usual spontaneous occurrence. The development of hypergammaglobulinemia and lymphoid cell hyperplasia in the young mice indicated that immunologically competent cells, derived from either the transplant or the recipient, proliferated during this process. These experiments, together with other findings, provide further support for the view that membranous glomerulonephritis in NZB/Bl mice is produced by immunological, and probably autoimmune, mechanisms and that the renal disease is apparently almost wholly unrelated to the hemolytic process.

Animals↗