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Biomedical subjects

R M Lewis

Publications and source records attributed to R M Lewis.

At least 217 records · Page 12Linked to original sources
PubMed1973

Prevention of murine lupus nephritis by carrier-dependent induction of immunologic tolerance to denatured DNA.

Four nucleosides were covalently bound to isogeneic mouse immunoglobulin G (IgG) and injected into New Zealand mice. Mice that received the tetranucleoside isogeneic IgG from birth to 5 months of age failed to make antibody to denatured DNA. In contrast, mice that were similarly treated with tetranucleoside bovine serum albumin or tetranucleoside free of carrier produced the same amount of antibody to denatured DNA as did untreated mice of this strain. Mice that were rendered tolerant to denatured DNA by tetranucleoside isogeneic IgG failed to develop the chronic membranous glomerulonephritis that characterizes the renal lesions in animals of this strain.

Adenosine↗
PubMed1973

Canine systemic lupus erythematosus. Transmission of serologic abnormalities by cell-free filtrates.

The presence of viruses was sought in a colony of dogs bred from parents with systemic lupus crythematosus (SLE). Cell-free filtrates prepared from the spleens of these animals were injected into newborn dogs, mice, and rats. The canine recipients developed antinuclear antibody (ANA) and positive lupus erythematosus (LE) cell tests: ANA and, in some cases, antinative DNA antibodies were produced by the murine recipients: no abnormalities were detected in the rats. Serial passage of spleen cells or cell-free filtrates of spleen tissue in syngeneic mice reduced the time required for appearance of ANA from 9 to 4 mo. Some murine recipients of the canine filtrate developed malignant lymphomas. Murine leukemia viruses were identified in these tumors by electron microscopic, virologic, and serologic technics. These neoplasms, but not other tumors known to contain murine leukemia viruses, were associated with the production of ANA. Puppies inoculated with the canine filtrate-induced mouse lymphoma developed ANA and positive LE cell tests within 4 mo. THE RESULTS WERE INTERPRETED TO INDICATE THE PRESENCE IN CANINE SLE OF A VIRUS CAPABLE OF: (a) inducing the serologic abnormalities of SLE in normal dogs and mice: (b) activating latent murine leukemia viruses: and (c) spreading by both horizonal and vertical routes.

Animals↗
PubMed1971

Canine systemic lupus erythematosus. Genetic analysis of an established breeding colony.

Three breeding lines, originating from dogs with SLE, have been established. Two lines were initiated by mating a female with SLE with a normal male. The third line resulted from a mating of two affected dogs. Brother-to-sister matings have reached the third generation in each line. In addition, backcross and outcross matings were carried out. More than one-third of the autopsied dogs had thymic abnormalities. The commonest lesion was a lymphoid follicle; the thymus of one dog contained multiple granulomas, and in one animal a reticulum cell sarcoma of the thymus was found. Multiple serological abnormalities, including positive LE cell tests, anti-nuclear antibodies (ANA), and rheumatoid factor, were found in the progeny. The development of ANA appeared unrelated to the incidence of positive LE cell tests. About 10% of the animals had rheumatoid factor in their serum. Control populations of dogs; including house pets; two other, unrelated lines of inbred dogs; and normal dogs housed in the same facility as the SLE colony did not have these abnormalities. The incidence of positive LE cell tests in the inbred, backcross, and outcross matings was not consistent with any conventional genetic mechanism of inheritance. It is conceivable that the results can be explained by vertical transmission of an infectious agent in a genetically susceptible individual.

Animals↗
PubMed1968

Chronic allogeneic disease. I. Development of glomerulonephritis.

Glomerulonephritis, often accompanied by the nephrotic syndrome, developed in CAF(1) mice following the administration of spleen cells from normal BALB/c mice. The renal lesion was membranous glomerulonephritis. When studied with fluorescein-conjugated antisera to either mouse gamma globulin or beta(1C)-globulin, the glomeruli contained beaded and irregular deposits of these immunoproteins. The ultrastructure of the lesion was characterized by thickening of the glomerular basement membranes and the presence of electron-dense subepithelial deposits. Acid eluates of the diseased kidneys contained gamma globulin that failed to bind to sections of normal kidneys. These findings conform to the type of nephritis provoked by immune complexes. They indicate that this type of immune injury can be based on the reaction of intolerant immunocytes to normal antigens.

Animals↗
PubMedDate not supplied

Changes in populations of immune effector cells during the course of haemorrhagic fever with renal syndrome.

To characterize the immune response in haemorrhagic fever with renal syndrome, serial changes in immune effector cells were measured in 14 patients. Significant findings included initial elevations of all major leucocyte populations, increases in suppressor T cells and B cells, decreases in helper/suppressor cell ratios, and a dramatic increase in activated T cells. These changes were most marked in severely ill patients. Changes reverted to normal over approximately one week.

Adult↗
PubMedDate not supplied

Platelet dysfunction contributes to the haemostatic defect in haemorrhagic fever with renal syndrome.

To characterize further the nature of haemostatic impairment in haemorrhagic fever with renal syndrome, we assessed platelet function in 9 patients in whom the diagnosis was serologically confirmed. Defective platelet aggregation was demonstrated in every patient. An abnormality of the granule release reaction was demonstrated in all of 7 patients tested. Gel-filtered platelets from a normal subject showed normal aggregation in plasma from a patient with impaired aggregation, which is evidence for an intrinsic platelet defect, and against the presence of a circulating inhibitor in this patient.

Adenosine Diphosphate↗