Virus-induced Cell Surface Antigens Research Articles

Moloney leukemia virus-induced cell surface antigen mimicry by monoclonal antibodies.

We have investigated antigen-independent modulation of immune responses by monoclonal antibodies directed against both viral and nonviral antigens. BALB/c mice were immunized with monoclonal IgM (i.e. Ab1) specific for either Moloney murine leukemia virus-induced cell surface antigen (MCSA) or the hapten 2,4-dinitrophenyl (DNP). Injection with either Ab1 activated a functional idiotypic (Id) network as evidenced by production of both anti-Id (Ab2) antibodies and anti-anti-Id (Ab3) antibodies. A subset of induced Ab3 (designated Ab1), exhibited specificity for antigen (virus or DNP). In mice immunized with anti-Id antibodies (Ab2), production of Ab3 and Ab1′ was also observed. In the MCSA system, antibody-induced Ab1′ responses were effective in protecting mice from tumor development upon subsequent challenge with live virus. Furthermore, antigen-independent modulation of immunity to both viral and nonviral antigens was found to be thymus-dependent. Similar findings in other viral systems suggest that antibody-induced activation of Id networks may prove a viable alternative vaccine strategy that can elicit antigen-specific responses, and in some cases protection, in the apparent absence of exposure to antigen.

Recognition of autologous lymphoblastoid cells by cloned human T cells: Inhibition of cytotoxicity by Anti-HLA antibody but not by antibody to Epstein-Barr virus induced cell surface antigen

Cytotoxic T cells (T c) can be primed in vitro to specifically kill autologous Epstein-Barr virus (EBV) transformed lymphoblastoid cell line cells (LCL). The antigen recognized by T c on the LCL cells is designated LYDMA (lymphocyte determined membrane antigen). Recognition of LYDMA may also require simultaneous recognition of HLA determinants. Despite its immunogenic potency, the genetic origin and molecular structure of LYDMA remains undetermined. Most LCL cells do not produce EBV virus, but all LCL cells appear to express an immunogenic, non-HLA class I, 47,000 Dalton determinant which is detected by several independently derived mouse monoclonal antibodies. This determinant is not readily detected on peripheral blood lymphocytes, nor on EBV-associated Burkitt's lymphoma cell lines. We examined the potential relationship between this 47,000 MW Epstein-Barr virus associated cell surface antigen (the EBVCS antigen) and LYDMA. Populations of T c generated by in vitro activation with irradiated autologous LCL cells were potent at destroying EBVCS bearing autologous LCL cells. The addition of anti-EBVCS antibody to this cytotoxic interaction had no suppressive effect. Furthermore, single cell derived, LYDMA reactive, T c clones able to specifically destroy autologous LCL were studied. Cytotoxicity could be inhibited by monoclonal antibody to HLA-Class I determinants, but not by monoclonal antibodies to EBVCS. Thus, these LYDMA reactive T c clones do not recognize the same antigenic determinant as the monoclonal antibodies specific for EBVCS. It remains uncertain whether this 47,000 MW glycoprotein that carries the serologically detected EBVCS antigen may be directly recognized by human T cells.

Occluded and Budded Autographa californica Nuclear Polyhedrosis Virus: Immunological Relatedness of Structural Proteins

The immunological relatedness of the structural proteins of the budded and occluded phenotypes of Autographa californica nuclear polyhedrosis virus was examined by reciprocal immunoblotting and by in situ peroxidase-antiperoxidase staining of virus-induced cell surface and intracellular antigens with antisera to both phenotypes. The molecular weights (MWs) of major structural proteins of both phenotypes that reciprocally cross-reacted were 92,500, 78,000, 62,500, 54,000, and 42,000. A highly immunogenic, major structural protein of the occluded phenotype of 46,000 MW was not recognized by antiserum to the budded phenotype, and a major structural protein of the budded phenotype, 48,000 MW, was not recognized by antiserum to the occluded phenotype. Both the budded and occluded phenotypes contained a protein of 33,500 MW that comigrated with polyhedrin (the matrix protein) and reacted with antiserum and monoclonal antibody to polyhedrin. Evidence was obtained for the apparent antigenic relatedness of proteins of different MWs from the budded and occluded phenotypes, possibly indicative of different processing of some proteins for the two phenotypes. Antiserum to the occluded phenotype recognized virus-induced cell surface antigens, indicating antigenic similarities between the occluded phenotype and envelope proteins of the budded phenotype. Antiserum to the budded phenotype recognized viral proteins produced before the appearance of cytopathic effect, whereas antiserum to the occluded phenotype did not.

Genetic control of sensitivity to Moloney leukemia virus in mice V. Role of H-2-linked genes in the control of anti-FMR cytolytic T lymphocytes

Three H-2-linked genes, Rmv1, Rmv2, and Rmv3 control the resistance of mice against Moloney virus (MLV)-induced leukemias. It has been shown previously that they function as immune response (Ir) genes regulating the level of antivirus antibodies. In the present experiments, the cell-mediated anti-tumor response has been studied in a series of inbred strains selected for their resistance or sensitivity to the MLV-induced disease. We failed to detect any relationship between resistance and sensitivity and the ability to produce cytolytic T lymphocytes (CTL) directed against the virus-induced FMR cell surface antigen. Furthermore, the role of each Rmv gene has been studied separately using congenic pairs of mice differing at only one of these loci: we failed to evidence any influence of these genes in the cell-mediated antitumor reactions as measured by the ability to lyse syngeneic FMR(+) target cells. Nevertheless a gene mapping in the D region of the MHC but probably different from Rmv3 controls the response of a subset of anti-FMR CTL restricted by the H-2K k antigens, with higher response in H-2D d than in H-2D b animals. This observation confirms the existence of H-2D region associated Ir genes regulating the CTL-mediated antitumor immune responses by choosing the subset of responder CTL, and suggests that a fourth H-2-linked gene plays some role in the genetic control of the anti-FMR immune response.

Mouse fibroblasts transformed by Rous sarcoma virus express a virus-specific non-virion transplantation antigen.

Rous sarcoma virus (RSV)-transformed fibroblasts from different animals species a serologically detectable virus-induced non-virion cell surface antigen (VCSA), whose expression is controlled by the transforming viral src gene and by a cellular gene. Now, by in vivo immunization, we have found that RSV-transformed fibroblasts from different mouse strains share a virus-specific transplantation antigen. In fact, only animals immunized with irradiated syngeneic or allogeneic fibroblasts transformed by RSV, but not animals immunized with cells transformed by different oncogenic agents, rejected a lethal dose of syngeneic RSV-induced tumor cells. Immunoprecipitation tests with monospecific antisera showed that the expression of this antigen did not correlate with the presence of intracellular viral proteins other than the src gene product pp60src. However, hyperimmunization of mice with hamster or quail fibroblasts transformed by RSV, that express a high level of pp60src, did not induce transplantation resistance. It is concluded that the expression of both the serologically-defined VCSA and the transplantation antigen is the result of the interaction of pp60src with host cell gene product(s) rather than the simple exposure of pp60src at the outer cell surface.

Continuous cell culture from chick embryos inoculated with rev strain t

Oncogenic reticuloendotheliosis virus strain T (REV-T) was inoculated into 9-day-old embryonated eggs of specific pathogen free chickens. A continuous cell line was established from the liver cells of one embryo harvested the day before hatching which had the following properties: It formed loose aggregates and propagated floating in the medium. The cell doubling time was about 24 hours. Viral antigen was demonstrated in the cytoplasm by the direct immunofluorescent antibody technique. C-type particles were observed outside the cells. Virus-induced cell surface antigen was demonstrated by the immunofluorescent antibody technique. The cell line grew in soft agar. Virus production continued in the cell line for 17 months. When the cells or the culture fluid were inoculated into 1-day-old chickens, they died from neoplastic disease. The chickens which survived after infection showed abnormal feathering ("nakanuke"). The virus released from this cell-line was inoculated into 9-day-old embryonated eggs and three cell lines were established. These cell lines did not contain avian leukosis/sarcoma viruses.

T lymphocyte tolerance and early appearance of virus-induced cell surface antigens in Moloney-murine leukemia virus neonatally injected mice.

Regression of Moloney-murine sarcoma virus- (M-MSV) induced sarcomas in normal adult mice is accompanied by generation of virus-specific cytotoxic T lymphocytes (CTL). However, when neonatal mice that were injected with Moloney-murine leukemia virus (M-MuLV carrier) were subsequently challenged as adults with M-MSV, the sarcomas did not regress nor did they generate CTL. This failure to produce CTL cannot be ascribed to nonspecific immunodepressive effects or to suppressor cell generation since M-MuLV carrier mice exhibit normal reactivity after allogeneic cell stimulation. Moreover, addition of M-MuLV-infected cells as the third party to cultures does not reduce activity of CTL from M-MSV immune mice. Since M-MSV and M-MuLV possess common antigens, the observed unresponsiveness was considered in relationship to induction of a T lymphocyte tolerance, which may follow introduction of foreign antigens at an early stage of development. In fact, it was observed that as early as 10 days after injection, thymus, lymph node, and spleen from M-MuLV carrier mice express virus-induced cell-surface antigens that not only are targets for M-MSV-immune CTL, but also induce in vitro a strong specific cytotoxic response. In addition, a cold target inhibition assay disclosed that the same antigens are shared by both M-MuLV infected and leukemia cells, even though they are less expressed on the surface of the former. The finding that the cytotoxicity of alloreactive lymphocytes from M-MuLV carrier mice is reduced after preincubation with M-MSV immune CTL confirms that virus infection does not bring about functional inactivation of lymphocytes. Finally, it was observed that virus antigen presence on lymphocytes from M-MuLV neonatally injected mice is closely related to subsequent leukemia development.

T cell-mediated immunity to oncornavirus-induced tumors. III. Specific and nonspecific suppression in tumor-bearing mice.

A strong cell-mediated immune response against Friend, Moloney, Rauscher virus-induced (FMR) cell surface antigens has been demonstrated previously in mice which reject oncornavirus-induced tumors. In order to identify an eventual suppressor mechanism in animals with progressively growing tumors, experiments were initiated in C57BL/6 mice bearing either a murine sarcoma virus (MSV) tumor or Moloney virus-induced lymphoma (MBL2). Progressive tumor growth was induced (a) in viremic animals first infected with Moloney murine leukemia virus (M.Mu LV), then inoculated as adult with MSV; (b) in nonviremic animals injected with MBL2 lymphoma cells. In the absence of tumor cells, viremia induces specific tolerance for which there is no evidence for suppressor cells. In tumor-bearing mice, specific suppressor T cells are detected which are able to inhibit the generation of anti-FMR cytolytic T lymphocytes in vitro and enhance the tumor growth in vivo. In addition to the specific suppressor T cells, a nonspecific suppressive activity mediated by metastatic T lymphoma cells is demonstrated in the spleens of lymphoma-bearing animals. The respective role of the virus and tumor cells in the induction of tolerance to M.MuLV-induced antigens, and their relationship to other components of the specific cell-mediated immune response is discussed.

Mutant analysis of herpes simplex virus-induced cell surface antigens: resistance to complement-mediated immune cytolysis.

BHK-21 cells infected with temperature-sensitive mutants of herpes simplex virus type 1 strain KOS representing 16 complementation groups were tested for susceptibility to complement-mediated immune cytolysis at permissive (34 degrees C) and nonpermissive (39 degrees C) temperatures. Only cells infected by mutants in complementation group E were resistant to immune cytolysis in a temperature-sensitive manner compared with wild-type infections. The expression of group E mutant cell surface antigens during infections at 34 and 39 degrees C was characterized by a combination of cell surface radioiodination, specific immunoprecipitation, and gel electrophoretic analysis of immunoprecipitates. Resistance to immune lysis at 39 degrees C correlated with the absence of viral antigens exposed at the cell surface. Intrinsic radiolabeling of group E mutant infections with [14C]glucosamine revealed that normal glycoproteins were produced at 34 degrees C but none were synthesized at 39 degrees C. The effect of 2-deoxy-D-glucose on glycosylation of group E mutants at 39 degrees C suggested that the viral glycoprotein precursors were not synthesized. The complementation group E mutants failed to complement herpes simplex virus type 1 mutants isolated by other workers. These included the group B mutants of strain KOS, the temperature-sensitive group D mutants of strain 17, and the LB2 mutant of strain HFEM. These mutants should be considered members of herpes simplex virus type 1 complementation group 1.2, in keeping with the new herpes simplex virus type 1 nomenclature.

Association of mouse adenovirus-induced cell surface antigen(s) with histocompatibility antigens.

AbstractThe topological relationship on the mouse adenovirus (M‐Ad)‐infected cell surface between virus‐induced specific cell surface(s) antigens and serologically defined major histocompatibility antigens (H‐2) was analyzed by the cap formation technique. Rhodamine‐isothiocyanate (RITC)‐labeled anti‐S serum failed to stain the surface of virus‐infected lymphoid cells which were pretreated with anti‐H‐2 serum and fluorescein isothiocyanate (FITC)‐labeled anti‐mouse immunoglobulin serum (anti‐M‐Ig) to cap the appropriate H‐2 antigens. Conversely, the capping of the S antigens by pretreatment with anti‐S followed by FITC anti‐M‐Ig serum induced cocapping of H‐2 antigens. The β2 microglobulins (β2m) were also shown to be cocapped with S antigens by anti‐β2m or by anti‐S serum. The S antigens, however, did not cocap with mouse‐immunoglobulins or Thyl. 2 antigens on virus‐infected B or T lymphocytes, respectively.To further elucidate the molecular relationship between S and H‐2 antigens, radio‐iodinated virus‐infected cells were solubilized with Nonidet P40 (NP40) and S antigens were precipitated with anti‐S serum. When the precipitates were analysed with sodium dodecyl sulfate Polyacrylamide gel electrophoresis, two major peaks were seen at positions of molecules of about 45,000 and 12,000 daltons both of which corresponded with molecules which were observed when NP40 extracts of virus‐infected or uninfected cells were precipitated with anti‐H‐2 serum. Sequential immunoprecipitation analysis of infected cell extracts showed that S antigens were coprecipitated with either H‐2K or H‐2D antigens. These results suggest that the S antigens are somehow associated with H‐2K or H‐2D antigens separately.

Antibody response to Moloney type C virus-induced tumours.

Animals infected with RNA tumour viruses show an immune response to new virus-induced antigens present on the tumour cell surface. In tumours induced by murine leukaemia virus (MuLV), serologically detected cell membrane antigens have been placed into two major groups; the Gross cell-surface antigen(s), GCSA and GIX, are associated with Gross leukaemia virus infection1 and the FMR antigen (s), associated with infection by Friend, Moloney or Rauscher type C viruses2. There is good evidence that some of these antigens are related to the structural proteins of the virus. The GIX antigen is found on the viral envelope protein, gp70 (refs 3–5) and the GCSA antigen is on the p30 protein which is present in the membrane as part of the glycosylated ‘gag’ polyprotein(s)6–8. It is not certain whether the FMR antigen(s) is found on membrane-located viral structural precursors or polyproteins, or whether it is present on a tumour-associated protein. Several antigens of this latter type have been described. For example, the Moloney leukaemia virus-induced cell-surface antigen (MCSA) is thought to be a non-viral protein associated with ‘gag’ products, p30, p15 and p12 on the membranes of Moloney lymphoma cells9,10. MCSA and the antigens on cells infected by Abelson MuLV11 may be very specific cellular antigens associated with Moloney MuLV infection. There has also been much interest in whether the src gene product is present in the membrane of sarcoma virus-induced tumours, although it is thought not to be present on the external membrane surface12. A more controversial point is whether there are other virus-induced cell-surface antigens (CSA) which may serve as targets for an effective immune response to viral tumours13. We have previously found14 that serum from BALB/c mice with regressed Moloney virus-induced fibrosarcomas contained specificities only for Moloney viral proteins and not for any tumour-associated protein like MCSA. We have now identified the viral proteins with which the Moloney MuSV antisera react. Using a syngeneic system of immunisation with freshly induced Moloney sarcoma tumours, we show that the antibody response is directed only at viral structural antigens and that the major part of the response is to antigens on p30 protein probably present as part of a precursor polyprotein on the tumour cell surface.

Antibody-induced modulation of Friend virus cell surface antigens decreases virus production by persistent erythroleukemia cells: influence of the Rfv-3 gene.

The Rfv-3 gene was found to influence the level of Friend leukemia virus production in spleens of leukemic mice later than 30 days after virus inoculation. Rfv-3r/s mice [(B10.A X A)F1 and (B10.A X A.BY)F1] had decreased spleen virus levels 30-90 days after virus inoculation compared to Rfv-3s/s mice [A.BY, A, BALB.B, and (BALB/c X A)F1)]. In (B10.A X A)F1 X A backcross mice the spleen virus titer segregated with the level of viremia. The Rfv-3 gene appeared to act by controlling anti-Friend virus antibody production. The interaction of antiviral antibody with infected cells led to a decrease in release of infectious virus by late leukemic spleen cells in Rfv-3r/s mice to 1/300th that in Rfv-3s/s mice. This decrease in virus release appeared to be due to interference with the virus budding process due to antibody-mediated modulation of virus-induced cell surface antigens.

Virus-induced cell surface antigens and cell-mediated immune responses

Virus-induced cell surface antigens and cell-mediated immune responses

Cell-surface antigens induced by RNA tumour viruses

Host animals show an immune response to the surface of cells infected with RNA tumour viruses. An element of this response is due to expression of viral structural antigens, but the major part is due to virus-induced cell-surface antigens (CSAs). This article compares the properties of CSAs of the avian, murine and feline retrovirus systems.

Moloney Virus-Induced Cell Surface Antigens and Histocompatibility Antigens Are Located on Distinct Molecules

Abstract The Moloney lymphoma, LSTRA, is widely used as a target cell for cell-mediated lysis studies. This report further characterizes the antigenic structures that may be important in the cytotoxic T lymphocyte-target cell recognition. Anti-H-2 sera have been absorbed to remove contaminating antiviral activity. The results presented demonstrate that: a) no linkage between H-2 and viral antigens was detected with 1-dimensional (SDS-PAGE) or 2-dimensional (IEF followed by SDS-PAGE) gel electrophoresis; b) no molecule showing the antigenic properties of both viral and histocompatibility antigens was detected; c) H2-Dd and H2-Kd molecules on the LSTRA lymphoma appeared antigenically similar to the parental BALB/c cells based on inhibition of cytotoxicity experiments; d) with cell extracts made in the presence of iodoacetamide, no disulfide linkages could be demonstrated between viral and histocompatibility antigens; e) the Moloney viral antigen gp70 was found in large amounts on the cell surface of LSTRA cells; f) the p30 precursor (gag) was not detectable on the cell surface, although it was abundant in the cell cytoplasm. Thus, these studies indicate that the LSTRA target cell appears to have H-2 and viral antigens present on separate molecules, which are dissociated during NP40 detergent extraction. No evidence was found of an “altered self” type molecule, in which either H-2 or viral antigens had been chemically altered as a consequence of viral transformation.

Immunization of mice with syngeneic Moloney lymphoma cells induces separate antibodies against virion envelope glycoprotein and virus-induced cell surface antigens.

Immunization of mice with heavily irradiated syngeneic Moloney lymphoma cells evokes antibodies against the major viral envelope antigen, gp71, and the Moloney virus-induced cell surface antigen (MCSA). A9HT cells, an L-cell subline, react with the antibodies against the viral envelope antigen only; this reaction can be completely inhibited by virus or purified gp71. Reactivity to Moloney lymphoma cells (YAC) was only partially inhibited (maximum 30%) or not at all. This can be attributed to the reaction of the YAC cells with antibodies directed against MCSA, a nonvirion cell surface component according to both biological and biochemical evidence. Antibody-induced capping of gp71 or p15(E) did not change the membrane distribution of MCSA or H-2, indicating that these antigens represent distinct entities on the cell surface. MCSA showed only minimal capping and thereby differed in behavior from both H-2 and virion antigens. gp71 could be capped by the mouse antiserum as revealed by subsequent staining with monospecific anti-gp71 antiserum. Under ordinary test conditions this reactivity is overshadowed by the reaction against MCSA. The lack of MCSA capping reflects a difference in anchorage of this antigen.

Moloney leukemia virus-induced cell surface antigen: detection and characterization in sodium dodecyl sulfate gels.

An experimental procedure for detecting and characterizing tumor-associated, virion, and histocompatibility antigens has been developed. The method takes advantage of the high resolution that proteins, solubilized by Triton X-100 and reduced, display after sodium dodecyl sulfate gel electrophoresis. The antigens can be detected as distinct molecular weight species by a highly sensitive inhibition of cytotoxic reaction. When coupled to the lactoperoxidase-catalyzed iodination of intact cells, the procedure permits the determination of externally exposed antigens. In the present study, the method has been applied to the Moloney leukemia virus-induced YAC lymphoma cells of strain A mice, which express a Moloney leukemia virus-determined cell surface antigen (MCSA) in addition to the type C viral proteins gp71, p30, p15, p15(E), p12, and p10. MCSA was identified as an exposed surface protein distinct in size and antigenic determinants from the major envelope and core protein of Moloney leukemia virus and the histocompatibility antigens. Multiple molecular weight species possessing antigenic determinants for MCSA, gp71, and H-2(a) have been detected. These results provide direct confirmation that MCSA is unrelated to the known virion structural proteins or to the H-2(a) antigen. This method should permit the direct identification and molecular weight characterization of any antigen whose determinants are not solely dependent on a complex quaternary structure and for which serological reagents are available.

Xenogenization of Rat Erythroid Cells by Lymphatic Leukemia Virus: Its Role in Induction of Autoimmune Hemolytic Anemia

Newborn rats given injections of low doses of Friend lymphatic leukemia virus subsequently developed hemolytic anemia characterized by production of antierythrocyte autoantibody. Electron microscopy showed C-type virus particles budding from the cell membrane not only of lymphoid cells but also of erythrocyte percursor cells in bone marrow and spleen, suggesting that the erythroid cells were infected by the virus. In addition, erythrocyte precursor cells expressed virus-induced cell surface antigens detected by cytotoxicity tests. Normal syngeneic rats preimmunized with a Friend lymphatic leukemia virusinduced tumor and subsequently inoculated with bone marrow, spleen cells, or reticulocyte-rich fraction derived from other rats injected with high doses of the virus at birth produced cytotoxic antibody to the virus-induced tumor and antierythrocyte autoantibody. In contrast, rats subsequently inoculated with virus-infected thymus or lymph node cells produced cytotoxic antibody but not antierythrocyte autoantibody. These results indicate that "xenogenization," previously shown for tumor cells and normal lymphoid cells, is also observed for rat erythroid cells and, further, that xenogenization of erythroid cells by Friend lymphatic leukemia virus is one of the most important factors in induction of autoimmune hemolytic anemia.

Autogenous immunity to endogenous RNA tumor virus: virion and virus-induced cell surface antigens.

Annals of the New York Academy of SciencesVolume 276, Issue 1 p. 343-357 AUTOGENOUS IMMUNITY TO ENDOGENOUS RNA TUMOR VIRUS: VIRION AND VIRUS-INDUCED CELL SURFACE ANTIGENS* J. D. Longstreth, J. D. Longstreth Basic Research Program, NCI-Frederick Cancer Research Center, Frederick, Maryland 21701 Predoctoral fellow of the Basic Research Program (FCRC). Portions of this manuscript will be submitted to UT-Oak Ridge Graduate School of Biomedical Sciences in partial fulfillment of a Ph.D. degree.Search for more papers by this authorJ. N. Ihle, J. N. Ihle Basic Research Program, NCI-Frederick Cancer Research Center, Frederick, Maryland 21701Search for more papers by this authorM. G. Hanna Jr., M. G. Hanna Jr. Basic Research Program, NCI-Frederick Cancer Research Center, Frederick, Maryland 21701Search for more papers by this author J. D. Longstreth, J. D. Longstreth Basic Research Program, NCI-Frederick Cancer Research Center, Frederick, Maryland 21701 Predoctoral fellow of the Basic Research Program (FCRC). Portions of this manuscript will be submitted to UT-Oak Ridge Graduate School of Biomedical Sciences in partial fulfillment of a Ph.D. degree.Search for more papers by this authorJ. N. Ihle, J. N. Ihle Basic Research Program, NCI-Frederick Cancer Research Center, Frederick, Maryland 21701Search for more papers by this authorM. G. Hanna Jr., M. G. Hanna Jr. Basic Research Program, NCI-Frederick Cancer Research Center, Frederick, Maryland 21701Search for more papers by this author First published: September 1976 https://doi.org/10.1111/j.1749-6632.1976.tb41659.xCitations: 2 * Research supported by the National Cancer Institute Contract NO1-CO-25423 with Litton Bionetics, Incorporated. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume276, Issue1International Conference on Immunobiology of CancerSeptember 1976Pages 343-357 RelatedInformation

Independence of Moloney virus-induced cell-surface antigen and membrane-associated virion antigens in immunoselected lymphoma sublines.

THE nature of virus-determined cell-surface antigens (CSAs), recognised by the syngeneic host on neoplastic cells induced by RNA viruses has not been properly defined in spite of much recent speculation about the possible role of cell membrane associated virion proteins1. Lymphoma cells induced by the Moloney leukaemia virus (MLV) are said to carry MCSAs. It is a matter of some debate whether MCSA is identical with the tumour-associated transplantation antigen (TATA) detected in vivo by the rejection of small tumour grafts in syngeneic preimmunised animals. Views are divided on the origin and control of CSA and/or TATA: some authors regard them as virally induced, but distinct from virion antigens (see for example refs 2–5) whereas others believe that they are virion components, inserted into the cell membrane6,7. Antisera against purified virion components (designated according to the recently adopted nomenclature8) have been used to demonstrate that p30 and gp69/71 are present on the surface of mammalian type C RNA virus-infected cells9–11. We have confirmed this in the present paper using an MLV-induced mouse lymphoma (YAC) and shown, in addition, that antigen(s) identical with or related to p15 and p12 are also expressed on the outer cell surface. Since these specificities were all detected with antisera produced in foreign species, the question as to which, if any of them, is responsible for MCSA, the antigen recognised by the syngeneic mouse—as mentioned above—remains open. We have approached this question by exposing the YAC lymphoma repeatedly to the immunoselective pressure of anti-MCSA sera and passage through preimmunised syngeneic hosts, until all detectable MCSA has disappeared. The immunoresistant sublines were compared with the original YAC line with regard to the expression of the various virion antigens. The results support that MCSA differs from the known virion antigens, partly or completely.