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S Ostrand-Rosenberg

Publications and source records attributed to S Ostrand-Rosenberg.

50 records · Page 3Linked to original sources
PubMed1986

402AX teratocarcinoma MHC class I antigen expression is regulated in vivo by Lyt 1, Lyt 2, and L3T4 expressing splenic T cells.

The murine 402AX teratocarcinoma is a MHC class I antigen negative tumor of 129 strain origin. Host resistance to the 402AX tumor is genetically controlled. When passed intraperitoneally in genetically resistant mice, the tumor cells are induced to express MHC Class I antigens of the 129 genotype. When passed in genetically susceptible mice, the tumor cells remain MHC class I antigen negative. Earlier studies have demonstrated that resistance to the tumor and regulation of tumor cell MHC class I antigen expression are under the control of the host's immune system. The present studies indicate that splenic Lyt 1-, Lyt 2-, and L3T4-expressing cells regulate tumor cell MHC class I antigen expression, and that these cells require a genetically resistant host environment in which to differentiate. Splenic T cells primed to the 402AX tumor and transferred into genetically susceptible 129 mice give rise to GVHD, suggesting that immunity to the tumor involves reactivity to 129 minor histocompatibility antigens.

Animals↗
PubMed1986

Teratocarcinoma cell MHC antigen expression is regulated in vitro by a soluble noninterferon factor.

The 402AX murine teratocarcinoma is a spontaneous testicular tumor of 129 (H-2b) origin which does not express MHC encoded antigens. Rejection of this tumor is immunologically mediated and the tumor cells are induced in vivo to synthesize H-2b antigens when passaged in genetically resistant host mice. The present studies demonstrate that serum from tumor primed genetically resistant host mice can induce tumor cell MHC antigen expression in vitro as measured by indirect immunofluorescence using monoclonal antibodies. The inducing factor is specific for 402AX tumor cells and is not interferon as shown by the lack of response of the 402AX tumor to gamma interferon, and the absence of significant interferon activity in inducer serum. These studies demonstrate another factor independent of interferon that can induce MHC class I antigen expression on tumor cells.

Animals↗
PubMed1984

Regulation of major histocompatibility gene expression in teratocarcinoma 402AX cells.

Teratocarcinoma 402AX cells are induced to express major histocompatibility complex (MHC) antigens when passaged in vivo in genetically resistant host mice. Studies reported here demonstrate that MHC antigen induction is regulated in vivo in part by the synergistic action of Lyt 1 and Lyt 2 positive splenic T cells and in vitro by serum from tumor-primed resistant mice. Northern blots suggest that some teratocarcinoma 402AX MHC class I antigens may be post-transcriptionally regulated.

Animals↗
PubMed1983

Multiple splenic lymphoid cell subpopulations regulate H-2 antigen expression on teratocarcinoma cells in vivo.

Undifferentiated murine 402AX teratocarcinoma cells do not express MHC antigens when passaged in vitro or in vivo in genetically susceptible host mice. When passaged in vivo in genetically resistant mice, however, the tumor cells become H-2b antigen positive regardless of the H-2 haplotype of the resistant host mouse. The present studies use monoclonal anti-H-2b antibodies to corroborate these earlier findings, which were performed with conventional antisera. Previous studies have established that host bone marrow plus lymphoid cells from resistant primed donors regulate tumor cell H-2b antigen expression. Using bone marrow and mature lymphoid cell reconstitution techniques, the present studies indicate that splenic Ig- cells from genetically resistant host mice are the most efficient lymphoid cell subpopulation in tumor cell H-2b antigen induction. Ig+ spleen cells also reconstitute the capacity to induce teratocarcinoma cell H-2 antigens but are less effective than Ig- spleen cells. Tumor cell H-2 antigen induction in C57BL/6 beige mice is impaired compared to C57BL/6 hosts, which suggests that host NK cells may also be involved in tumor cell H-2 antigen induction. Reconstitution of lethally irradiated resistant hosts for teratocarcinoma cell H-2 antigen expression requires bone marrow plus resistant primed lymphoid cell subpopulations; bone marrow alone is insufficient. These results indicate that multiple splenic lymphoid cell subpopulations requiring a radiosensitive host environment and/or factor for differentiation regulate teratocarcinoma 402AX H-2b antigen expression in vivo in genetically resistant mice.

Animals↗
PubMed1981

H-2 antigen expression on teratocarcinoma cells passaged in genetically resistant mice is regulated by lymphoid cells.

Previous studies have demonstrated that resistance and susceptibility to the 402AX testicular teratocarcinoma are under genetic control in the mouse. Under normal culture conditions or when passaged in genetically susceptible hosts, the nullipotent 402AX cells do not express H-2 antigens. However, when passaged in genetically resistant animals, the tumor cells become strongly positive for H-2 antigens in the absence of other indications of differentiation. These studies suggested that H-2 antigen modulation on teratocarcinoma cells is mandatory for an effective host cell-mediated immune response against this tumor. The present studies further examine the role of H-2 antigen modulation on teratocarcinoma cells and determine which host cell populations are mediating H-2 modulation on the tumor cells. Reconstitution of lethally irradiated susceptible hosts with resistant bone marrow extends the mean survival time of the host but does not confer complete resistance. Teratocarcinoma cells passaged in such reconstituted hosts do not express H-2 antigens. Two lines of evidence suggest that H-2 antigen modulation is mediated by lymphoid cells: (i) sublethal irradiation of genetically resistant hosts inhibits H-2 antigen modulation on teratocarcinoma cells passaged in vivo and (ii) immunological priming can overcome the loss of H-2 modulation that is normally associated with aging in genetically resistant hosts. Genetically susceptible mice can be fully reconstituted for tumor rejection and H-2 antigen expression on teratocarcinoma cells by reconstitution with genetically resistant bone marrow plus lymphoid cells from tumor-primed resistant hosts. These results: (i) imply the necessity for H-2 antigens on tumor cells for an effective host cell-mediated immune response against the tumor, and (ii) indicate that host lymphoid cells regulate H-2 antigen expression on tumor cells passaged in vivo.

Animals↗
PubMed1981

H-2 negative teratocarcinoma cells become H-2 positive when passaged in genetically resistant host mice.

The murine 402AX teratocarcinoma is an H-2 negative, nullipotent stem cell tumor of testicular origin. Previous studies have demonstrated that host strain resistance and susceptibility to this tumor are under the control of 2 genes, one of which is closely linked to the mouse major histocompatibility complex. Earlier studies determined the lack of antigenic modulation and the absence of H-2 antigens on 402AX cells passaged in vitro or in genetically susceptible hosts. The present studies demonstrate that when passaged in genetically resistant host mice [C57BL/10, B10.SM, and B10.129(6M)], the H-2 negative 402AX cells modulate to become positive for H-2b antigens, as detected by indirect immunofluorescence, microcytotoxicity, and quantitative absorption. Two to 4 days of in vivo growth in resistant hosts is necessary for H-2b antigens to be expressed. H-2 positive tumor cells removed from resistant hosts and placed in culture become H-2 antigen negative within 1 to 4 hr in vitro. H-2 antigen turn-on on the teratocarcinoma cells is specific for the H-2 haplotype of the tumor cell origin (129, H-2b); alien H-2 antigens are not expressed. The observation that only teratocarcinoma cells growing in genetically resistant hosts turn-on for H-2 antigens suggests that major histocompatibility antigens on target cells are required for an efficient host cell-mediated immune response against tumor cells.

Absorption↗
PubMed1980

Detection of the circulating antibodies to teratocarcinomadefined antigens in patients with testicular tumours.

Sera from twenty-three patients with primary or metastatic testicular tumours of germinal origin were tested for antibodies against teratocarcinoma-associated antigen(s), using an indirect immunofluorescence technique. Human and 129/Sv mouse sperm and mouse teratocarcinoma cell line 402 AX were used as target cells. A total of fifteen sera were identified as positive, six of them when tested against both sperm and tumour cells. Tail staining has been the most prevalent pattern of fluorescence on both human and murine spermatozoa. These observations suggest that antibody to a common teratoma-defined antigen(s) was detected in sera of patients with testicular tumours.

Adult↗
PubMed1975

Gene dosage and antigenic expression on the cell surface of bovine erythrocytes.

Electron microscopic and serological techniques have been used to study the relationship between cell surface expression of bovine erythrocyte antigens and the genes coding for these antigens. Using cells which are genetically and serologically defined for their zygosity with respect to the Z allele, it was found that homozygous (Z/Z) cells have approximately twice as much surface Z antigen as heterozygous (Z/-) cells. Cells labeled for the J antigen, a soluble serum substance which secondarily adsorbs to the erythrocyte surface, display a quantity of antigen which is directly related to the J titer of the cells. A new antigen is described which is independent of the J antigen, and which is detectable by EM labeling and by indirect agglutination, but not by hemolysis.

Animals↗
PubMedDate not supplied

Transfection of major histocompatibility complex class I and class II genes causes tumour rejection.

Many human and mouse tumours do not express MHC class II antigens and have reduced levels of class I antigens. Because of the requirement for class I and/or class II antigen for antigen presentation to Th and Tc cells, these phenotypes may enable tumour cells to 'escape' the host's immune response. Experiments presented here are designed to assess the role of MHC class I and class II antigens in tumour immunity, and to overcome the MHC class I- or class II-negative phenotype. When transfected with the syngeneic H-2Db gene, the MHC antigen-negative 402AX teratocarcinoma expresses high levels of H-2Db antigen. 402AX/Db cells are rejected by MHC allogeneic and some MHC syngeneic 402AX-susceptible mice, however the fully syngeneic strain of origin (129) remains tumour-susceptible. Induction of MHC class I gene products on class I antigen-negative embryonal carcinoma cells therefore increases tumour immunogenicity in some hosts, but not in the fully syngeneic mouse. In an attempt to enhance antigen presentation of tumour-associated antigens to Th cells, MHC class I antigen-positive SaI (KkDd) sarcoma cells were transfected with syngeneic A alpha k and A beta k genes to generate Iak-expressing tumour cells. SaI/Ak cells are efficiently rejected by syngeneic A/J (KkDd) mice, while untransfected SaI cells are lethal. Induction of MHC class II antigen expression on the class I antigen-positive SaI sarcoma therefore completely abrogates malignancy.

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