Publications by authors named "MILGROM F"

Ethanol-soluble, but saline-insoluble antigens were prepared as saline suspensions and studied in double diffusion reactions in a soft agarose gel. Positive reactions were observed with syphilis and SLE sera tested against the Kahn antigen as well as against commercial cardiolipin reagents. Also, ethanol-soluble brain antigen was studied for organ-specific reactions with rabbit immune sera.

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Previous studies on the appearance in pathological human sera of antibodies to an antigen of normal mammalian organs were continued. In gel precipitation reactions, antibodies combining with saline extracts of mammalian organs were found in 20 of 63 cancer sera and in 4 of 15 syphilis sera, but only in 3 of 56 other pathological sera. Furthermore, an identical antigen was demonstrated in 5 of 58 pathological sera.

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Introduction: Previous numerous papers by the senior author dealt with the human serum factor referred to as anti-antibody which is specifically directed against IgG antibodies that underwent molecular transformation in the course of the reactions with their corresponding antigens. The reactions of this serum factor could be conveniently detected by means of agglutination of Rh-positive erythrocytes sensitized by anti Rh antibodies. No precipitation tests could be developed.

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Agglutination tests with preparations of parenchymatous organs were developed. The tissue suspensions were dried at room temperature after they had been spread as a very thin layer on a glass plate, or otherwise, they were lyophilized. The dried preparations were pulverized and then prepared as stable suspensions in saline.

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It was noted that many sera of patients with renal allograft produce distinct precipitation lines in gel diffusion tests with about 20% of infectious mononucleosis sera. The antibodies in infectious mononucleosis sera were of IgM isotope, but, interestingly, they could be removed by guinea pig kidney homogenate, which indicated that the reactions studied were of the Hanganutziu-Deicher rather than of the Paul-Bunnell type. This contention was strengthened by the fact that positive transplantation sera reacted also with standard serum with Hanganutziu-Deicher antibodies.

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Quail-chicken spinal cord chimeras are a model for temporary acceptance followed by rejection of xenografts and also for demyelinating lesions of the central nervous system. The antiglobulin test with quail erythrocytes was employed to detect antibodies in sera of quail-chicken spinal cord chimeras. Sera of all 46 chimeras tested gave positive results.

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Spinal cord chimeras were constructed by orthotopic grafting of quail embryonal neutral folds, neural crest and neural tube into chicken embryos. The spinal cord xenografts were accepted for varying lengths of time, but most chimeras eventually rejected the quail transplant. This was associated with perivenular cuffing and demyelination with preservation of most neurons, as well as clinical neurological symptoms.

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The pathogenesis of streptococcus-induced nephritides (SIN) involves immune complex-mediated inflammation; however, specific mechanisms are still poorly understood. Using preparations of two strains of Streptococcus mutans (SM) in attempts to induce SIN in rabbits, one preparation was strongly and the other virtually not nephritogenic. The non-nephritogenic preparation provided a negative control for our studies.

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Forssman antigen is a glycosphingolipid with antigenic specificity determined by extra-membrane haptenic sugars similar to blood group antigens and antigens that are the main barrier to xenogeneic organ transplantation. Herein, we describe the localization of Forssman antigen in guinea pig lungs and kidneys and the consequences of its interaction with antibodies in vitro and in vivo (Forssman reaction). Exposure of cultured guinea pig aortic endothelial cells to Forssman antibodies induced rapid redistribution of antigen-antibody complexes at the cell surface, followed by shedding that occurred by blebbing of plasma membrane as vesicles or fragments, and was associated with disappearance of antigen from the cell surface (antigenic modulation).

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Availability of a line of rabbits deficient in the sixth complement component (C6-D) made it possible to evaluate the role of the terminal complement complex (TCC) in the development of experimental autoimmune thyroiditis (EAT) of the rabbit. Immunization with saline extract of homologous thyroid, known to be composed predominantly of thyroglobulin, led in normocomplementemic (NC) rabbits to severe thyroiditis, with cellular infiltrates occupying 50-95% of the thyroid, and to minimal or moderate thyroiditis, with 1-35% of thyroids infiltrated in C6-D rabbits. Cellular infiltrates consisted predominantly of mononuclear cells with appreciable numbers of granulocytes.

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The role of autoantibodies in the pathogenesis of autoimmune thyroiditis (AT) still remains poorly understood. Serum transfer experiments in experimental AT (EAT) and spontaneous AT (SAT) animal models frequently did not succeed or only resulted in minor thyroid lesions. The inconsistent results may have arisen because of technical problems inherent in serum transfer, the major of which is to obtain high enough concentrations of autoantibodies over long enough periods at the potential site of tissue injury.

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Immunization of rabbits with physicochemically altered homologous or even autologous IgG induces formation of antibodies combining with IgG of rabbit and of foreign species. Cardiac but not renal lesions were reported in such animals. This study examined the nephritogenic potential of the immune response to cationized or heat-aggregated homologous IgG of b9 or b4 allotype in rabbits of the b4 allotype.

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Spinal cord chimeras were produced by replacing a small fragment of neural tube of a 2-day-old White Leghorn chicken embryo with a similar fragment from a Japanese quail embryo. The embryo mortality was 61%, and 72% of hatched birds were 'cripples' and had to be sacrificed within 5 days after hatching. Forty-nine chimeras, 10.

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During studies of agglutination of trypsinized human red blood cells (RBC) by anti-Rh sera, it was noticed that some human sera without Rh antibodies agglutinated these erythrocytes. Of 933 normal and pathological sera subsequently screened, 116 produced such agglutination. The agglutinins were of IgM nature and were directed against an antigen exposed or created by tryptic digestion of RBC.

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A previous study described clinical and pathological manifestations observed in 49 chimeras produced by replacing a small fragment of the neural tube of a chicken embryo by a similar fragment from a Japanese quail embryo. Predominant antibodies in sera of these birds were directed against xenogeneic antigens which are devoid of organ specificity and which are present in quail tissues but absent from chicken tissues. Mixed agglutination test with quail cell monolayers detected such antibodies in sera of all chimeras tested.

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(C57BL/6 x A/J)F1 murine recipients of DBA/2 kidney allografts developed tolerance to DBA/2 tissues, which was measured by observation of growth of a DBA/2 tumor. Eleven, 14 and 18 days after inoculation, the size of the tumor was considerably larger in kidney-grafted than in nongrafted animals. Still, the susceptibility of grafted animals to the tumor did not equal the susceptibility of the DBA/2 mice syngeneic with the tumor.

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After left nephrectomy, 3 10-week old NZB/W mice received orthotopic grafts of kidneys from parental NZW mice of the same age. At autopsy conducted at the age of 33-38 weeks, glomerulonephritis of similar extent was noted in the recipients' own and in the grafted kidneys. Also, very similar granular deposits of immunoglobulins and complement were demonstrated in these kidneys.

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Murine renal allografts were studied using (C57BL/6J x A/J)F1 mice as recipients and DBA/2 mice as donors. In this strain combination, protracted rejection was noted in that the circulation was maintained in the graft for over 10 weeks. In all grafts examined after 3 weeks, mononuclear cell infiltrates were noted; in addition, all grafts had immune deposits, apparently containing transplantation antibodies, in glomeruli, tubuli and vessels.

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The study involved a monoclonal rheumatoid factor referred to as RF-AN, obtained by Steinitz and his associates from IgG-reactive human lymphocytes 'immortalized' by infection with Epstein-Barr virus. RF-AN combined with red blood cells (RBC) sensitized by either human or rabbit IgG antibodies. The monoclonal character of RF-AN strongly suggested that the same molecule of this factor combined with IgG of both species.

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