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PubMedDate not supplied

Study of cell surface antigens induced by herpes simplex virus. Note II. Some properties of the antigens.

Surface antigens induced by herpes simplex virus infection in HeLa cells remain unaltered after treatment of the cells with 2% formalin for 10 min or with 0.08% trypsin for 15 min at 37 degrees C. A longer trypsin treatment (for 1 hour) will cause gradual alterations in the virus-induced antigens. Hence, these antigens are proteins deeply implanted within the cellular membrane. Their mobility--optimal at 37 degrees C--allows aggregation of the antigens in the form of caps or patches by polyvalent ligands such as IgG.

Antigens, Surface↗
PubMed1979

Regulation of surface antigen expression in Paramecium primaurelia. II. Role of the surface antigen itself.

In the wild-type strains, 156 and 168, of Paramecium primaurelia, the alleles G156 and G168 expressed at medium temperature specify two immunologically distinguishable surface antigens 156G and 168G, whose phenotypic expression shows allelic exclusion, the majority of heterozygotes being phenotypically [156G] while a small minority is phenotypically [156G-168G]. At high temperature, the antigens coded by another locus, generally the D locus, are expressed. This system, displaying both intergenic and interallelic exclusion, provides favourable material to analyze the respective roles of the genome, of the antigens expressed and of the environmental conditions, in particular temperature, on the regulation of the expression of surface antigens. This analysis was carried out by studying the variations of the expression of surface antigens as a function of temperature, culture medium and previously expressed antigens in different genetic situations (a) in homozygotes: the wild-type strains 156 and 168, and the isogenized strains "G156 isogenic 168 carrying the G156 allele in a 168 genetic background; (b) in heterozygotes of the two phenotypic classes of heterozygotes, [156G] and [156G-168G]. The results show that (1) the thermal stability of the expression of a given surface antigen and its rate of re-appearance at the cell surface depend on its own specificity; (2) in heterozygotes [156G-168G], the stability of the expression of the antigen 156G is modified and "adjusted" to that of the less stable surface antigen 168G, and (3) the surface antigen itself exerts a positive control on the maintenance of its own expression. An interpretative model of "transmembranous control" is proposed to account for the regulation of the expression of surface antigens in Paramecium.

Alleles↗
PubMed1979

Simultaneous occurrence in the same serum of hepatitis B surface antigen and antibody to hepatitis B surface antigen of different subtypes.

The simultaneous occurrence of hepatitis B surface antigen (HBsAg) and antibody to HBsAg (anti-HBs) of different subtypes in the serum of a hemodiaylzed patient was studied. The w(a) subdeterminants were involved. The HBsAg belonged to the ayw3 subtype, and the anti-HBs exhibited monospecific anti-w2 activity. Both the HBsAg and the anti-HBs were detectable by counterelectrophoresis (CEP). The specificity of the antibody was demonstrated by CEP in tests against 128 sera containing HBsAg of 12 different subtypes and in absorption experiments with eight sera containing HBsAg of eight different subtypes, as well as by radioimmunoassay in the liquid phase. The monospecific antibody was selectively directed against the w2 subdeterminant of the adw2 subtype and was designated anti-w2.

Absorption↗
PubMed1977

Necrosis of the hepatocytes with hepatitis B surface antigen. Occurrence in a chronic hepatitis B surface antigen carrier.

Light and electron microscope finding from a liver of a chronic carrier of hepatitis B surface antigen (HBsAg) showed small lymphocytes and macrophages in close contact with liver cells, partial lysis of variable degrees, lytic necrosis, and the complete loss of a few hepatocytes with HBsAg in the cytoplasm. On the basis of these findings, together with the results from immunofluorescence study, the pathogenesis of hepatitis B is discussed, with emphasis on the importance of host cellular immune response. The cytopathic and cytolytic activities of immunologically activated T lymphocytes against liver cells that have antigenic targets associated with HBsAg at their surface and in the cytoplasm are discussed.

Adult↗
PubMed1978

Studies on cell surface antigens of mouse leukemic and normal lymphocytes. I. Categories of cell surface antigens on mouse leukemia and their serological identification.

Analysis of cell surface antigens is most advanced with mouse tumors, mainly because of the availability of inbred strains with known susceptibility to naturally occuring or induced tumors. The development of serological techniques enables identification of gene products which are expressed on the surface of tumor cells. The naturally occuring and induced leukemias in mice are a particularly suitable model for the studies of surface antigens, because the leukemia cells can be easily obtained in cell suspension, they are highly sensitive to cytotoxic antibodies and they can be compared, because of common origin, with normal thymocytes and lymphocytes. In addition to conventional alloantigens (MHC), differentiation alloantigens (Thy, Tl and Lyt) viral structural (MuLV and occasionally MMTV) also viral related cellular antigens are detectable. Various categories of cell surface antigens and antisera defining their presence on the surface of mouse lymphocyte produced and used for studies carried on in the Department of Tumor Immunology are listed and discussed in the present and following papers (No. I-V).

Animals↗
PubMed1978

[E antigen (HBeAG) and surface antigen (HBsAg) in bladder schistosomiasis].

The problem of the relationship between surface B antigen and schistosomiasis or other parasitic infections which are transmitted though the skin is not still resolved. Serum samples from 54 Somalian patients infected by Schistosoma haematobium were tested for the presence of the surface B antigen (HBsAg) and the e-antigen (HBeAg). The HbsAg was found in 14.8 per cent of these patients, while among controls (47 cases) the frequency was of 34.0 p]er cent; no e-antigen was found among the patients and controls, the prevalence of anti-HBs antibodies was of 57.4 per cent among the patients with urinary schistosomiasis and of 44.6 per cent among the controls; a low rate of anti-e antibodies was found in the patients (7.4%) and in the controls (10.6%). These observation seem to indicate that the problem of an increased frequency of hepatitis B virus markers among patients with urinary schistosomiasis needs for further investigation.

Adolescent↗
PubMed1977

Biochemical studies of the common and restricted antigens, two neural cell surface antigens.

Two cell surface antigens on rat neural tumor cells are defined by antisera from mice immunized with a rat glioma cell line, 33B. The Common antigen is on rat brain and embryo, and is strongly expressed on the surface of all, or most, rat glioma and neuroblastoma cell lines and tumors. The other Restricted antigen is not present at detectable levels on normal rat tissues, but is on 33B, and on 11 other rat neural tumors or cell lines developed from such tumors, though many other tumors are negative. These 2 antigens are on cell membrane preparations from cells and tumors, and have been further characterized using a quantitative antigen assay. Both antigens are heat labile, and can be destroyed by digestion with proteolytic enzymes. The Common antigen is 10 times more sensitive than the restricted antigen to pronase digestion. Furthermore, spacially separate sites for the 2 antigens are indicated by blocking experiments with pepsin digested antisera. Attempts to purify these antigens further have been frustrated by loss of antigenic activity upon detergent-induced release from the membrane. The tissue and tumor distributions of recently described mouse and rat surface antigens are reviewed. Many of these antigens are present on both brain and kidney, but not on other tissues, though several are shared with embryonic cells or sperm. Several new antigens have been described which may be neuronal specific.

Animals↗
PubMed1976

Cell surface antigens. IV. Immunological coorespondence between glycophorin and the a1 human cell surface antigen.

A stable human-Chinese hamster ovary cell hybrid has been produced which, in addition to the complement of Chinese hamster ovary (CHO-K1) chromosomes, contains only one human chromosome, No. 11. The human cell-surface antigens whose expression is controlled by human chromosome 11, and are expressed by this hybrid, have been defined as the AL immunogenetic complex. Although one component of this immunogenetic complex (a1) is also expressed by human red blood cells, a second component (a2) is not. Killing of an a1+ hybrid by anti-a1 serum and complement can be completely inhibited by glycophorin, the major glycoprotein component of the human erythrocyte membrane. In the presence of complement, antiserum prepared against glycophorin will kill only those cells which express a1. The anti-a1 killing activity of the anti-glycophorin can be absorbed out only by those cells which express a1. Therefore, it is concluded that the a1 cell-surface antigen has at least one antigenic component in common with glycophorin.

Adsorption↗
PubMed1977

Fractionation on lymphocyte surface antigens. I. Rapid method for eliminating labeled lipid from cell surface antigens iodinated by the lactoperoxidase catalysed reaction.

Fractionation of lactoperoxidase iodinated cell surface material on miniature DEAE-cellulose columns provided a rapid method for separating labeled lipid from cell surface antigens. The procedure also removed poorly solubilized aggregates yielding a labeled preparation which demonstrated stable, reproducible immunoprecipitation results. Using these fractionated antigens components tentatively designated as human 'T' cell specific antigens have been identified.

Antigens↗
PubMed1978

Cell-mediated immune response to liver tissue antigen and hepatitis B surface antigen after infection with hepatitis B virus in humans.

The in vitro correlates of cell-mediated immunity to liver tissue antigens and hepatitis B surface antigen (HBsAg) were studied in groups of subjects with acute and chronic hepatitis B virus (HBV) infection and in a population of HBV-seronegative controls. The technique of in vitro lymphocyte transformation (LTF) was employed in these studies. No LTF response to liver-specific antigen and HBsAg was observed in the control population. LTF activity in response to HBsAg was present in 11 of the 14 subjects with acute type B viral hepatitis during the early phase of the disease, and eight of these subjects also had LTF reactivity to liver antigen. During the convalescent phase the LTF reactivity to these antigens usually disappeared. More than 70% of patients with chronic carriage of HBsAg who had elevated levels of liver enzymes showed LTF responses to HBsAg, and a significant number of these subjects also exhibited LTF response to liver-specific antigen. On the other hand, chronic HBsAg carriers who persistently showed normal liver enzyme values (asymptomatic carriers) failed to show significant responses to liver antigen or HBsAg. It is suggested that the persistence of cellular reactivity to liver antigens may lead to the establishment of chronic liver disease.

Acute Disease↗
PubMed1977

Relationship between E receptors and a T-specific surface antigen on human T cells.

The aim of this study was the delineation of different antigenic surface determinants on the surface of adult peripheral T cells by means of a specific horse anti-human T-cell serum (ATS). It was shown that this serum reacts both with E receptors and (an) additional T antigen(s). While E receptors showed the already known susceptibility to trypsin, T antigens (as demonstrated in cytotoxicity tests) were resistant to trypsinization even at high concentration. Incubation of the trypsinized peripheral blood lymphocytes (PBL) in 5 per cent CO2 allowed the resynthesis of E-receptors. High concentrations of ATS (without complement) significantly inhibited rosette-formation. This suggests a close steric relationship between E receptors and T antigen(s). However, absorptions of ATS with trypsinized PBL left the E-rosette inhibitory capacity unaltered. Treatment of PBL with ATS in appropriate dilutions and indirect immunofluorescence tests under capping conditions followed by conventional rosette procedures showed that the E receptor and T antigens are separately mobile within the T-cell membrane.

Antigens↗
PubMed1977

Genetics of cell-surface antigens: regional mapping of three components of the human cell-surface antigen complex, AL, on chromosome 11.

Cytogenetic analysis has been performed on a series of deletion mutations on human chromosome 11 of AL hybrid clones in which specific markers have been lost as a result of treatment with mutagenic agents. Such analysis has localized the three previously identified components of the AL cell-surface antigen complex to the indicated regions of chromosome 11: a1 and a3:11p13 leads to 11pter; a2:11q13 leads to 11qter. Using these methodologies human lactic dehydrogenase A localization on the short arm as reported by others has been confirmed. Evidence is presented provisionally assigning this gene to 11p13 leads to 11pter.

Antigens↗
PubMed1978

Demonstration of a surface antigen on Epstein-Barr virus genome-carrying lymphoid cells: distinction from the virus-determined membrane antigen.

A surface antigen (SA) was detected on Epstein-Barr virus (EBV)-carrying lymphoid cell lines by indirect membrane immunofluorescence with an antiserum from a rabbit immunized with Raji cells; the antiserum had been extensively absorbed with normal human blood and tonsil cells. The SA was not detected on normal human umbilical cord and adult peripheral blood lymphocytes or EBV-negative cell lines. Incidences of the SA and EBV-determined membrane antigen (MA) on certain EBV-carrying cell lines were not compatible. Antibody against SA was differentially absorbed by the SA-positive MA-negative cell lines whereas MA antibody was absorbed by MA-positive SA-negative cell lines. The results of cross-absorption tests of antiserum against Raji cells or P3HR-1 cells suggested that SA may contain more than one antigenic determinant.

Absorption↗
PubMed1977

Alteration of cell-surface antigenicity of the mouse plasmacytoma. II. Lack of correlation between synthesis of myeloma protein and alteration of surface antigen.

The correlation between the changes of immunoglobulin synthesis and the surface antigenicity was analyzed by cytotoxicity and quantitative antibody-absorption tests with the cells of immunoglobulin-producing and nonproducing mouse plasmacytoma. IgA-synthesizing BLAB/c plasmacytoma 58-8 and the non-IgA-synthesizing variant of the 58-8 (nonproducer) were killed with rabbit anti-58-8 plasmacytoma cell antiserum, C3H/He anti-BALB/c spleen cell antiserum, and (C57BL/6 X DBA/2)F1 anti-BALB/c plasmacytoma cell MOPC-31C antiserum plus complement, only when the cells were pretreated with pronase. Quantitative absorption tests revealed that the nonproducer, 58-8 had the same amount of plasmacytoma antigen of 58-8 and PC.1 antigen, and a greater amount of H-2d antigen, as did producer 58-8. The same analysis was carried out for the C3H mouse plasmacytoma X5563, which has an M-component of IgG2a. The nonproducer X5563 had a greater amount of H-2k antigen and a smaller amount of the plasmacytoma antigen of X5563 than did the producer X5563. No detectable PC.1 antigen was observed at surfaces of the producer and the nonproducer X5563 cells.

Animals↗
PubMed1976

Induction of GIX antigen and gross cell surface antigen after infection by ecotropic and xenotropic murine leukemia viruses in vitro.

A number of ecotropic and xenotropic murine leukemia viruses were examined for their ability to induce the GIX antigen and Gross cell surface antigen (GCSA) in tissue culture fibroblasts. GIX appears to be a constituent of murine leukemia virus gp70; a molecular characterization of GCSA has not yet been reported. Antigen induction was measured by the ability of productively infected cells to absorb cytotoxic activity from the standard GIX- and GCSA-typing antisera. Cells infected by ecotropic viruses displayed four distinct phenotypes GIX:+/GCSA++, GIX-/GCSA++, GIX++/GCSA+, and GIX-/GSCA+; cells infected by xenotropic viruses were either GIX-/GCSA+ or GIX-/GCSA-. GIX induction appeared to be a type-specific property of some but not all Gross-AKR type ecotropic viruses. Differences in the degree of absorption of the GCSA antiserum by ecotropic virus- and xenotropic virus-infected cells indicated that GCSA may comprise multiple antigenic determinants.

AKR murine leukemia virus↗
PubMed1975

Alteration of cell-surface antigenicity of the mouse plasmacytoma. I. Immunologic characterization of surface antigens masked during successive transplantations.

Alterations of membrane antigenicity of IgA-synthesizing plasmacytoma cells (58-8) induced in a BALB/c mouse were investigated with rabbit antisera against 58-8 transplanted from 7-8 generations (anti-58-8) and mouse antisera against H-2d (anti-H-2d). The 58-8 cells transplanted (TP) for 8 generations (TP8), showed moderate susceptibilities to anti-58-8 [cytotoxicity index (CI) = 72%] and to anti-H-2d (Cl = 30-40%). At TP12, the susceptibility to anti-58-8 remained (tCl approximately 50%) but there was none to anti-H-2d (Cl = 0-10%). After TP13, 58-8 cells had detectable reactivity neither with anti-58-8 nor with anti-H-2d before proteolysis. However, antigenicity was demonstrated after treatment of cells with proteases: Anti-58-8 and anti-H-2d became cytotoxic to pronase-treated 58-8 (P-58-8) and these cytotoxic reactivities of antisera could be completely absorbed with P-58-8- but not with "intact" 58-8. Anti-H-2d absorbed with P-58-8 had no cytotoxicity to BALB/c spleen cells. Absorption of anti-H-2d with BALB/c spleen cells did not show any measurable cytotoxicity to P-58-8. Appearance of antigenicity after proteolysis was transient and reversible. When P-58-8 was incubated in vitro, susceptibilities to antisera were decreased. Actinomycin D and puromycin inhibited the loss of susceptibility; these metabolic inhibitors suppressed the "masking" of antigenic determinants with protein-like material(s). In early generations (TP8), 58-8 cells were susceptible to antiserum to bone marrow-derived lymphocytes (anti-B) and complement. The cells completely absorbed the cytotoxicity of anti-B against spleen cells. After additional transplantations (TP14, TP30), susceptibilities to anti-B were no longer detectable and no removal of the cytotoxicity was shown, though the cells were pretreated with pronase. Anti-B failed to kill MOPC-31C.

Animals↗
PubMed1978

Molecular association between transplantation antigens and cell surface antigen in adenovirus-transformed cell line.

A rat cell line (A2T2C4) transformed with adenovirus type 2 elicited cytotoxic T lymphocytes in syngeneic rats. Cytotoxicity was abolished by a rabbit antiserum directed against the major histocompatibility (AgB) antigens and by a syngeneic rat antiserum raised against the virus-transformed cell line. The syngeneic antiserum immunoprecipitated surface proteins with apparent molecular weights of 45,000, 19,000, 17,000, and 12,000 from the A2T2C4 cells but it displayed no reactivity against primary rat fibroblasts and spleen cells. The rabbit antiserum against AgB antigens precipitated a 19,000-dalton component from the A2T2C4 cells which was not observed in primary rat fibroblasts. Sequential immunoprecipitation revealed identity between the major polypeptides recognized by the two antisera. Because the rabbit anti-AgB antigen serum was specific for the transplantation antigen subunits and because the syngeneic rat antiserum against the A2T2C4 cells failed to react with the AgB antigens in normal cells, it is concluded that the 19,000-dalton component is coprecipitated with the AgB antigens. Antisera directed specifically against beta2-microglobulin and the alloantigenic AgB antigen subunit also coprecipitated the 19,000-dalton component. These results indicate that the AgB antigen subunits form a ternary complex with a virus-coded protein on the surface of the virus-transformed A2T2C4 cells. This molecular complex may be recognized by the cytoloytic T lymphocytes

Adenoviruses, Human↗