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Biomedical subjects

J Ivanyi

Publications and source records attributed to J Ivanyi.

At least 181 records · Page 10Linked to original sources
PubMed1981

Allotype suppression in the chicken. III. Analysis of the recovery form suppression by neonatally injected or maternal antibodies.

Injection of M-1 (Cmu), G-1 (Cgamma) heterozygous chickens on the day of hatch with anti-IgM-1 antiserum induced allotype suppression from which chickens recovered over a period of approximately 4 months. The suppression of the serum IgM-1 levels was matched by a decrease in the number of splenic and peripheral blood B cells bearing the relevant IgM-1 allotype, and a compensatory increase in the number of cells bearing the alternative nonsuppressed IgM-1 allotype. However, the proportion of IgM-1 bearing bursal cells was only marginally altered. The recovery from suppression was due to B cell recruitment and could be abrogated by bursectomy. Allotype suppression induced in ovo or maintained by repeated injection of anti-IgM-1 anti-serum resulted in chronic suppression and depletion of the relevant peripheral as well as bursal IgM-1-bearing cells. Antibody titers of the relevant allotype in partially suppressed chickens generally correlated with serum allotype levels without clonal restriction in antibody response of the suppressed allotype.

Animals↗
PubMed1981

Allotype suppression in the chicken. IV. Deletion of B cells and lack of suppressor cells during chronic suppression.

Embryonally induced allotype suppression in M-1,G-1 heterozygous chickens was stable for at least 18 months after hatching. Suppression was established rapidly since injection of antigen only 4 days after anti-IgM-1 antiserum failed to abrogate its effect. Injected chickens had undetectable serum levels (i.e. less than 40 micrograms/ml) of the suppressed IgM-1 and low (0.3-0.6 mg/ml) levels of the linked IgG-1 allotype. This correlated with a complete depletion of cells bearing the relevant IgM-1 allotypes and a compensatory increase in the alternative nonsuppressed IgM-1 allotype-bearing cells in the spleen, peripheral blood and bursa. Cell transfer studies suggested that suppression could not be attributed to allotype-specific suppressor cells.

Animals↗
PubMed1980

Genetic polymorphism of a serum euglobulin of chickens which binds to antigen-antibody complexes.

Binding of a euglobulin from normal chicken serum to precipitating HSA anti-HSA complexes has been demonstrated. The binding appeared specific for the Fc-fragment of chicken antibody since it was not detected with rabbit Ag-Ab complexes. Two allelic allotypic markers of the euglobulin under genetic control from one locus (E-1) were found in chickens from two inbred strains. E-1 alleles segregated independently from those controlled by the B (major histocompatibility), M-1 and G-1 (Ig allotype) loci. Partially purified E-1 had a sedimentation coefficient of 15.6 S. and beta-globulin electrophoretic mobility.

Animals↗
PubMed1980

The induction of suppressor T cells by concanavalin A is independent of cellular proliferation and protein synthesis.

Factors that govern the induction of suppressor T cells after stimulation with concanavalin A (Con A) were investigated in a two-stage culture system. Normal mouse spleen cells were incubated with Con A in the presence of a variety of drugs and then assayed for suppressive activity by means of a secondary anti-sheep erythrocyte response in vitro. The inclusion of inhibitors of mitosis (vinblastine sulphate or mytomycin C) or protein synthesis (cycloheximide or pactamycin) into normal spleen cell cultures containing Con A failed to inhibit the subsequent development of suppressor cells. Furthermore, spleen cells from mice previously irradiated with 900 rad or injected with cyclophosphamide expressed a level of suppressor activity after Con A stimulation which was equivalent to that of normal spleen cells. However, the inclusion of drugs that inhibit microtubule or microfilament function (colchicine or cytocholasin B) did prevent suppressor cell induction. Kinetic studies also revealed that significant suppressor activity was detectable in normal spleen cells after only 3 h exposure to Con A. These results indicate that the induction of suppressor T cells in this system is a maturation event involving changes in the cell membrane and is entirely independent of protein synthesis and cellular proliferation.

Animals↗
PubMed1980

Pathogenesis of virus-induced osteopetrosis in the chicken.

Infection of chicken embryos with a nondefective avian leukosis virus MAV-2(0) induced bone hyperplasia and profound suppression of bursal and thymic lymphoid cell development within 2- to 3 weeks after hatching. A time-course study of infectivity during embryonal life showed a gradual loss of susceptibility between the 10th day of incubation and hatching. This finding suggests that an embryonal stem cell either before or early after seeding into the bone and primary lymphoid organs is a virus-susceptible target cell. Histologic observations of the bursa indicated only mild damage during the 1st week and severely impaired proliferation of follicular lymphoid cells during subsequent weeks of development. Thus, viral infection conferred a cytostatic rather than a cytolytic effect upon the lymphoid target cell. Infection of stem cells, which are progenitors of lymphoid cells as well as of bone osteoclasts, is compatible with the manifestations of the disease. A model of cellular disorders of the bone and lymphoid tissues is proposed. Adoptive transfer of lymphoid cells from adult MAV-2(0)-immunized chickens into histocompatible virus-infected juvenile recipients abrogated the manifestation of osteopetrosis. Passive injection of antiserum containing virus-neutralizing antibodies was also effective. Anti-gp85 viral surface glycoprotein-binding antibodies in sera from adoptively protected chickens receiving immune cells were exclusively of cell donor IgG allotype.

Animals↗
PubMed1978

Acquired heterophile antigens on the surface of human cell lines.

Chicken IgM antibodies raised against sheep erythrocytes (SE) reacted with a heterophile carbohydrate antigen designated as "HC". This antigen was visualized by SE rosette formation with antibody-sensitized and formaldehyde-fixed target cells. Cells from eight lymphoblastoid lines and ten lines of diverse histogenetic origin all expressed HC on their surface to a greater or lesser degree when grown in fetal calf serum (FCS). Lymphoblastoid cell lines, HSB2 and Namalva, lost most of their HC antigen after three cell divisions when grown in medium which contained normal human serum (NHS) instead of FCS. The acquired origin of HC was demonstrated by the conversion of HSB2-HC- into HSB2-HC+ cells after incubation in the presence of FCS or fetuin for 18 h at 37 degrees C. The acquisition of HC antigen depended on the concentration of fetuin as well as the time and temperature of incubation. The presence of NHS in the culture medium reduced the degree of HC incorporation. The level of HC expressed on the cell surface was reduced by treating HSB2 cells with sodium periodate but not by proteolytic enzymes. Competitive inhibition with hog blood group substance and sheep IgG suggested similar specificity of HC on target cells which had been sensitized with either fetuin or sheep IgM (Eur. J. Immunol. 1977.7:204). The avidity of chicken antibodies to HC in either of these systems was several orders of magnitude lower than the binding to SE.

Antigens, Heterophile↗
PubMed1978

Antagonism between donor and host B cells in allotype congenic chicken chimeras.

B cell chimerism was analyzed in juvenile chickens given injections of major histocompatibility complex-compatible lymphoid cells. The allelic products of donor and host-derived B cells were monitored with antisera directed against M1 (IgM) and G1 (IgG) isotype-specific allotypes. Injection of peripheral blood lymphocytes and spleen cells suppressed host allotype levels whereas purified T lymphocytes were ineffective. Pretreatment of recipients with cyclophosphamide was more effective than irradiation in promoting both engraftment and host B cell suppression. Host allotype suppression endured for several months after cell transfer and was attributable to B cell deletion, as ascertained by the lack of cells which expressed surface M1. In partially suppressed chickens, host G1 was inhibited to a greater degree than M1 allotype. Host recovery was followed by donor B cell rejection when low numbers of donor cells and/or inadequate host conditioning was used. Selective M1 chimerism occurred when limiting numbers of spleen cells were transferred into cyclophosphamide-treated hosts, whereas selective G1 chimerism resulted after the transfer of large numbers of peripheral blood lymphocytes or spleen cells into unconditioned recipients. We consider that these findings can be attributed to a B cell surveillance mechanism which may be similar to that postulated previously to explain resistance to haemopoietic and tumour cells.

Animals↗
PubMed1978

Allelic exclusion of M1 (IgM) allotype on the surface of chicken B cells.

The membrane expression of M1 (IgM) and G1 (IgG) allotype markers on peripheral blood lymphocytes was examined by immunofluorescence. In homozygous chickens 15% lymphocytes stained with either anti-M1 or with polyspecific rabbit anti-Ig serum, suggesting that M1 is expressed on the surface of probably all B lymphocytes. In heterozygous M1a/M1b individuals antisera against either allelic antigens reacted with 50% of the total surface Ig positive cells as evidence for the allelic exclusion of surface M1 expression. Donor allotype synthesis was determined from serum allotype levels in congenic cyclophosphamide-treated recipients of lymphoid cells. Treatment of cells with anti-M1 serum prior to transfer inhibited both M1 and G1 allotype synthesis. The treatment of heterozygous (M1a/M1b, G1a/G1e) cells with anti-M1b serum inhibited specifically the synthesis of M1b and G1e allotypes controlled by linked genes from the same parental chromosome. Thus, B cells which had been the targets for anti-M1 antibody mediated suppression are also subject to allelic exclusion.

Animals↗