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Results for “Histocompatibility”

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PubMed1998

Experimental study of the histocompatibility of covered expandable metallic stents in the trachea.

STUDY OBJECTIVES: To evaluate the histocompatibility of four different materials used to cover expandable metallic stents. DESIGN: Prospective, randomized, unblinded study. SETTING: Animal research laboratory of Kurume University. PATIENTS OR PARTICIPANTS: Twenty 12- to 18-kg mongrel dogs. INTERVENTIONS: Handmade Gianturco-type stents with six bends, 20 mm in length, and 15 to 20 mm in diameter were covered using four different materials: polypropylene mesh, silicone-coated mesh, polyester mesh, and ePTFE. Covered stents were inserted into the trachea after i.v. anesthesia. Five animals were used in each group. MEASUREMENTS AND RESULTS: Postinsertion status was observed using clinical and bronchoscopy measures 7, 14, 28, and 56 days after intervention. Eight weeks after stent insertion, the tracheal specimens were studied pathologically. A scoring system was used to evaluate the histocompatibility of covered stents in each study group. The mean of clinical scores in the polypropylene group was 1.84+/-0.36, which was significantly higher than those in the groups of silicone, polyester, and ePTFE. The means of histopathologic scores in the polypropylene group and the silicone group were 1.60+/-0.55, which were significantly higher than those in groups of polyester and ePTFE. CONCLUSIONS: Polypropylene mesh cover was more suitable than silicone-coated mesh, polyester mesh, and ePTFE because of its excellent histocompatibility.

Anesthesia, Intravenous↗

PubMed2004

A novel HLA-A*3303-restricted minor histocompatibility antigen encoded by an unconventional open reading frame of human TMSB4Y gene.

Female-to-male hemopoietic stem cell transplantation (HSCT) elicits T cell responses against male-specific minor histocompatibility (H-Y) Ags encoded by the Y chromosome. All previously identified H-Y Ags are encoded by conventional open reading frames, but we report in this study the identification of a novel H-Y Ag encoded in the 5'-untranslated region of the TMSB4Y gene. An HLA-A*3303-restricted CD8(+) CTL clone was isolated from a male patient after an HSCT from his HLA-identical sister. Using a panel of cell lines carrying Y chromosome terminal deletions, a narrow region controlling the susceptibility of these target cells to CTL recognition was localized. Minigene transfection and epitope reconstitution assays identified an 11-mer peptide, EVLLRPGLHFR, designated TMSB4Y/A33, whose first amino acid was located 405 bp upstream of the TMSB4Y initiation codon. Analysis of the precursor frequency of CTL specific for recipient minor histocompatibility Ags in post-HSCT peripheral blood T cells revealed that a significant fraction of the total donor CTL response in this patient was directed against the TMSB4Y epitope. Tetramer analysis continued to detect TMSB4Y/A33-specific CD8(+) T cells at least up to 700 days post-HSCT. This finding underscores the in vivo immunological relevance of minor histocompatibility Ags derived from unconventional open reading frame products.

5' Untranslated Regions↗

PubMedDate not supplied

Antigen perception by T lymphocytes. Influence of the major histocompatibility complex.

There is considerable evidence that T cell activation to soluble antigens occurs only if this is processed by macrophages and displayed appropriately on the plasma membrane in association with products of the genes of the major histocompatibility complex. The genes responsible differ according to the antigens involved. For cytotoxicity, targets and killer T cells must share K or D region gene products. For delayed type hypersensitivity to fowl gammaglobulin in mice, I-A identity is necessary; for dinitrofluorobenzene, identity at either the I, K or D region is sufficient. Experiments using three different approaches do not support the notion that these genetic constraints are due to the necessity for the T cell and stimulator cell to match an identical gene product or "cell interaction molecule." Rather they favour the hypothesis that activated T cells recognize antigen and products of genes of the major histocompatibility complex. The implications of the results are discussed in terms of the mode of action of immune responsiveness (Ir) genes and of the possible parallel evolution of T cell receptors for antigen and gene products of the major histocompatibility complex.

Animals↗

PubMed1976

Immunosensitivity and histocompatibility antigens in drug-altered leukemic cells.

New antigenic properties of experimental lymphomas have been reported previously following in vivo treatment with antitumor agents. 5-(3,3-Dimethyl-1-triazeno)imidazole-4-carboxamide (DIC) induced new antigenic characteristics on L1210 and L5178Y lymphomas, that were previously investigated in studies in animals compatible with the original untreated parental tumors. Here the L1210/DIC and L5178Y/DIC susceptibility to the cytotoxic effects of allogeneic and xenogeneic lymphocytes and sera obtained from animals sensitized to DBA/2 histocompatibility antigens were studied. The original and the DIC tumors showed the same sensitivity to anti-DBA/2 cellular and humoral cytotoxicity. The immune response electied in allogeneic mice by the original and DIC sublines was evaluated by in vitro cell-mediated and humoral cytotoxic assay. Beyond the immune response to histocompatibility antigens, a specific, anti-DIC-antigen immunoreaction was not found. Inhibition assay of the cell-mediated cytotoxicity and absorption of the humoral cytotoxicity demonstrated that DIC-induced antigens are not reciprocally related in cell-surface concentration to the natural DBA/2 histocompatibility antigens associated with tumor cells of DIC lines. An experiment was conducted in which specific activity against the DIC-treated L5178Y/DIC cells was observed with anti-L5178Y/DIC rabbit immune serum absorbed with the parental L5178Y lymphoma. This finding provides additional support to previous studies indicating that treatment with DIC induced new antigens on the lymphoma cells.

Animals↗

PubMed1991

Class II histocompatibility antigen expression by cellular components of vitreous and subretinal fluid in proliferative vitreoretinopathy.

Proliferative vitreoretinopathy (PVR) is the major cause of failure in retinal detachment surgery. It is characterized by the formation of membranes extending along both surfaces of the detached retina and within the vitreous, but the nature of the growing cells has not yet been determined. Using cytologic and immunocytologic procedures with 13 different monoclonal antibodies directed against Class II histocompatibility antigens and various markers of epithelial and immunocompetent cells, 30 specimens were studied of vitreous or subretinal fluid removed from patients with PVR. Five main types of cells could be identified: heavily pigmented cells, poorly pigmented ones, large totally unpigmented macrophage-resembling ones, smaller unpigmented cells, and lymphocytes. Analysis of intravitreal pigment granules, using autofluorescence by epiillumination and cytologic procedures, showed two different populations of pigmented cells: one with autofluorescent lipofuscin granules and the other with exclusively melanin pigment. Immunostaining procedures confirmed the epithelial nonmacrophage lineage of the intravitreal and subretinal cells because most of these cells were positive for cytokeratin but negative for macrophage markers. In addition, 40-100% of these epithelial-derived cells strongly expressed Class II histocompatibility antigens HLA-DR and -DQ. Lymphocytes were found in 13 specimens; B-cells were seen, but no T-lymphocytes could be identified. These results confirm the involvement of retinal pigment epithelial cells and the strong morphologic changes they undergo during the course of PVR. Moreover, the expression of Class II histocompatibility antigens by the growing cells may be related to inflammatory phenomena, but their eventual role in the development and the extension of periretinal proliferation has not been determined.

Adolescent↗

PubMed1979

Histocompatibility antigens in patients with hepatocellular carcinoma and their relationship to chronic hepatitis B virus infection in these patients.

Although hepatocellular carcinoma is probably caused by one or more environmental carcinogens, a genetically determined susceptibility to the development of the tumor has not been excluded. In looking for such a predisposition, we have compared the histocompatibility antigens (HLA) of 102 southern African blacks with histologically proved HCC with those of 208 healthy blacks. The standard two-stage lymphocyte microcytotoxicity method was used to test for 40 antigens: 17 in the A locus, 20 in the B locus, and 3 in the C locus. None of the HLA antigens had a frequency that was significantly different in the patients and the controls. A close association undoubtedly exists between chronic hepatitis B virus infection and hepatocellular carcinoma. If this virus is proved to be oncogenic with respect to hepatocellular carcinoma, a genetic predisposition to the hepatitis B virus carrier state may have an indirect bearing on the etiology of the tumor. Sera from the hepatocellular carcinoma patients were therefore tested for hepatitis B virus markers (HBV surface antigen and antibody against HBV core antigen), and these were related to the patients' histocompatibility antigens. None of the HLA antigen frequencies was significantly different in the surface antigen-positive and the surface antigen-negative patients. As 88% of the patients were anticore positive, no meaningful correlation could be carried out with this marker. Analysis of histocompatibility antigens thus failed to show evidence of a genetic predisposition either to hepatocellular carcinoma or to chronic hepatitis B surface antigenemia in patients with this tumor.

Adult↗

PubMed1989

[Ontogeny of T-cell recognition of self histocompatibility antigens: parenteral influences].

The existence of parental influences on the recognition of self histocompatibility was investigated. The results obtained showed that: 1) fetal liver and neonatal splenocytes and thymocytes from F1 mice differed in their capacity to regulate parental alloreactive T reactions against self histocompatibility antigens either of maternal or paternal origin. Fetal and neonatal F1 cells--until day 5--were able to suppress systemic and local GvH reactions induced in F1 hosts with maternal but not with paternal splenocytes; 2) this differential regulatory activity concerning parental GvH reactions against self histocompatibility antigens are correlated with the existence of a differential time lag in the appearance of thymic contrasuppressor activity on maternal anti-paternal and paternal anti-maternal GvH reactivity; 3) splenocytes from reciprocal F1 hybrids--from day 14 onwards--differed in their ability to stimulate F1 T cell proliferation in SMLC reactions; 4) foster nursing of F1 hybrids on mothers from the paternal strain was able to induce permanent alterations in the ability of their splenocytes to stimulate the proliferation of responder F1 T cells. The stimulatory ability of splenocytes from foster-nursed hybrids was indistinguishable from that observed in the reciprocal F1 combination nursed by their own mother, suggesting that lactation would be involved in the differences registered; 5) reciprocal F1 mice differed in their response to conventional antigens presented in the context of parental Ia antigens, lactation also being responsible for the induction of these differences. The different mechanisms involved in the alterations of the outcome of self recognition in the litter are discussed.

Animals↗

PubMed1989

Potentiation of interferon induction of class I major histocompatibility complex antigen expression by human tumor necrosis factor in small cell lung cancer cell lines.

The response of class I major histocompatibility complex antigen expression to in vitro administration of interferon and tumor necrosis factor alpha (TNF-alpha) was measured using class I major histocompatibility complex-deficient small cell lung cancer cell lines. Significant induction also was observed using gamma interferon (IFN-gamma) alone, whereas TNF-alpha alone yielded only modest induction. Classic small cell lung cancer cell lines NCI-H146 and NCI-H209 best demonstrated synergistic HLA and beta 2-microglobulin antigen induction with IFN-gamma and TNF-alpha with the following dose schedule: 3-6 days of TNF-alpha (200 units/ml) followed by 48 h of IFN-gamma (100 IU/ml). Induction was quantitated using an 125I-Protein A radioimmunoassay. Synergistic induction of the HLA and beta 2-microglobulin surface antigens on NCI-H146 was also possible with alpha interferon and TNF-alpha but required a higher concentration of the interferon, i.e., 3-6 days of TNF-alpha (200 units/ml) followed by 48 h of alpha interferon (1000 units/ml). Small cell lung cancer cell line NCI-H146 was further studied for expression of major histocompatibility complex messenger RNA using the optimal doses and sequence of addition of IFN-gamma and TNF-alpha as indicated above. A significant induction with IFN-gamma alone and synergistic induction with both IFN-gamma and TNF-alpha was quantitated for both HLA-A2 and beta 2-microglobulin transcripts using Northern blot analysis. Incubation with relatively low subcytotoxic doses of IFN-gamma and TNF-alpha also resulted in a marked synergistic decrease in c-myc message.

Animals↗

PubMed1989

How important is histocompatibility in bone marrow transplantation?

The main issue addressed at the Fifth International Workshop on Bone Marrow Transplantation for Leukaemia was the importance of the major histocompatibility complex (MHC) and of minor histocompatibility (minor H) systems in allogeneic bone marrow transplantation (BMT) in humans. It is well established that mismatching for either HLA or minor antigens increases the risks of graft-versus-host disease (GVHD) and graft failure. In HLA-identical sibling transplants minor antigen differences may be responsible for these problems, which might be reduced by matching for minor antigens and improving methods for immunosuppression in vivo. If a suitable family member is not available, then a 'matched' unrelated donor (MUD) may be an alternative. At present MUD transplants have greater risks of GVHD and graft failure and consequently poor survival than HLA-identical sibling transplants; this may be due to unrecognized MHC polymorphisms or to multiple minor H differences. Possible strategies to improve the results of MUD transplants include better HLA matching, new in vitro functional tests for optimizing donor selection and better immunosuppression. Approaches for improving HLA typing include isoelectric focusing for class I and RFLP/allogenotyping or oligonucleotide typing for class II antigens. One obvious disadvantage of exploiting more precise methods for donor matching is the possibility of excluding donors with biologically unimportant histocompatibility differences, which would increase rather than reduce the proportion of patients without donors in a given panel. Functional assays could help in selecting donors on the basis of 'intelligent mismatching' within the HLA system.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1977

Analysis of the major histocompatibility complex in Syrian hamsters. III. Cellular and humoral immunity to alloantigens.

Among the genetic loci incorporated into the major histocompatibility complex in every species studied to date have been prominent genes encoding for strong histocompatibility determinants that elicit detectable alloantibody responses and which are the chief antigenic targets of cell-mediated cytotoxicity reactions. The K and D regions of the H-2 complex in the mouse and the A, B, and C regions of the HLA complex in man are representative examples. Syrian hamsters, as described in this report, do not make alloantibodies to antigens of this type and only very poorly do they carry out in vitro cell-mediated cytotoxicity to target cells putatively bearing these antigens. Since hamsters are quite capable of discriminating analogous antigenic differences in xenogeneic species, and xenogeneic sources cannot distinguish immunologically between the antigens encoded by the two hamster major histocompatibility alleles. Hm-1a and Hm-1b, we conclude that the hamster strains we work with are serologically indistinguishable by the methods used here. However, they obviously differ for determinants which elicit T cell-mediated responses, as evidenced by their ability to express acute skin graft rejection, mixed lymphocyte reactivity, graft-vs-host reactions, and cell-mediated cytotoxicity reactions. Such alloreactivity may reflect a mutation at an SD locus, affecting antigenic sites recognized only by T cells, or that the available hamster strains are SD identical, but differ at loci similar to the I region loci in mice. Alternatively, we cannot exclude the possibility that Syrian hamsters somehow fail to express properly the genes coding for SD determinants.

Animals↗

PubMed1987

Induction of class I major histocompatibility complex antigens in human teratocarcinoma cells by interferon without induction of differentiation, growth inhibition, or resistance to viral infection.

The behavior of human teratocarcinoma cells, and especially their stem cells (embryonal carcinoma cells), may provide insights into the properties of human early embryonic cells. We report here that human recombinant gamma-interferon (IFN-gamma) induced the expression of major histocompatibility complex Class I (HLA-A, B, C) antigens and beta 2-microglobulin in the two human embryonal carcinoma cell lines, 2102Ep cl.4D3 and NTERA-2 cl.D1, and in the yolk sac carcinoma cell line, 1411H; human recombinant IFN-alpha and IFN-beta were less effective inducers of these cell surface molecules. No induction was observed in the gestational choriocarcinoma cell line, JAR. Neither IFN-alpha, IFN-beta, nor IFN-gamma caused growth inhibition, expression of major histocompatibility complex Class II (HLA-DR) antigens, resistance to viral (vesicular stomatitis virus) infection, or expression of 2',5'-oligo(A)synthetase in any of the cells. Also, IFN-gamma neither induced differentiation of NTERA-2 cl.D1 cells, which are pluripotent human stem cells, nor influenced their differentiation induced by retinoic acid. However, developmental regulation of responsiveness to IFN was evident, since IFN-gamma induced higher levels of surface expression of HLA-A, B, C and beta 2-microglobulin in the retinoic acid-induced differentiated NTERA-2 cl.D1 cells than in the undifferentiated parental cells. Also, 2',5'-oligo(A)synthetase was inducible in the NTERA-2 cl.D1 differentiated cells by IFN-alpha and -beta, although not by IFN-gamma, and slight resistance to vesicular stomatitis virus infection was evident in aged cultures of differentiated cells exposed to IFN-alpha. The effect of recombinant mouse IFN-gamma on major histocompatibility complex expression by several murine teratocarcinoma cells was also examined: H-2 Class I (H-2Db), but not class II (I-Ab), antigens were induced in the parietal yolk sac carcinoma lines, PYS and F9Ac cl.9; in cultures of PCC3/A/1 containing both embryonal carcinoma (EC) and differentiated cells; and in cultures of the EC cells, PCC4azaR and PCC4AO, without evidence of differentiation. No induction was observed in the murine EC cell lines, F9 or FA (H-2Kk). Our results indicate that human EC cells, like murine EC cells, exhibit only a partial response to the interferons, and that the extent of this response is developmentally regulated.

Antigens, Surface↗

PubMed1985

Graft-vs-host reactions (GVHR) across minor murine histocompatibility barriers. I. Impairment of mitogen responses and suppressor phenomena.

In our laboratory, we have developed a murine model to examine GVHD across minor histocompatibility antigens. In our model, GVHD is induced by injecting B10.D2 spleen cells into irradiated BALB/c recipients. Seven to 10 days after irradiation and injection of cells, there are significant changes in cell function in the recipient spleens. In the B10.D2----BALB/c (600 rad) model, recipient spleen cells are profoundly unresponsive to Con A and LPS stimulation but show increased B cell activity measured by Staphylococcus aureus protein A plaque-forming activity. Spleen cells from such GVH mice profoundly suppress the mitogenic responses of normal BALB/c or B10.D2 spleen cells to Con A and LPS. The degree of impairment of the mitogenic response and the ability to suppress normal cells is proportional to the dose of cells used to induce GVH reactions. Both the inability to respond to mitogens and the capacity to suppress are also related to the dose of irradiation given to the recipients. In addition, immunosuppression across minor histocompatibility antigens shows an unevenhandedness. If we inject parental B10.D2 or BALB/c cells into F1 recipients (P----F1), there is greater inhibition of mitogenic responses when B10.D2 parental cells are given than when BALB/c cells are given to the irradiated F1 recipients. These experiments show that significant immunosuppression occurs during GVH reactions across minor histocompatibility barriers. The degree of suppression varies according to the dose of cells used to induce GVH, the dose of irradiation to the recipient and the "strength" of the GVH recognition system. Such experiments provide models for GVH disease seen in humans who receive treatment for leukemia or other diseases that involves recipient irradiation and infusion of HLA-identical bone marrow.

Animals↗

PubMed1987

[Delayed-type hypersensitivity to minor histocompatibility antigens and its genetic restriction].

The analysis of skin allograft survival time and the level of delayed-type hypersensitivity (DTH) reaction to major and minor histocompatibility antigens revealed the correlation between these parameters of the transplantation immunity. The data obtained have shown that histocompatibility in several non-H-2 antigens induces DTH reaction comparable with the reaction caused by H-2 antigens. The effector phase of DTH to non-H-2 antigens is H-2 restricted. No restriction of the afferent phase is revealed. The application of these results to the analysis of the mechanisms of the recognition of minor histocompatibility antigens in DTH is discussed.

Animals↗

PubMed1982

Class I major histocompatibility gene products of the brown Norway rat display two major antigenic regions.

Sixteen Lewis anti-Brown Norway monoclonal antibodies and sera from alloimmunized Lewis rats were used to study the topographic relationships of antigenic determinants on class I major histocompatibility gene products. Only two independent antigenic regions were identified in competition binding assays. The first region is composed of a set of overlapping epitopes that are conserved in class I major histocompatibility products of mice and humans, as well as rats. In contrast, the second antigenic region appears in a restricted number of inbred rat strains and is not detected in other species. The data provide serologic confirmation, at the monoclonal and serum alloantibody level, of conserved polymorphisms in the major histocompatibility gene products of different species, a finding that is consistent with the amino acid sequences of these molecules.

Animals↗

PubMed1984

Suppressor T cell recognition of major and minor histocompatibility alloantigens: selected suppression of MHC-directed responses by minor alloantigen Ts.

The induction of suppression by i.v. administered alloantigens in the murine host was analyzed as a model of the possible effects of blood transfusion on transplant survival. The results indicated that suppressor T cells (Ts) specific for minor histocompatibility alloantigens could be readily induced by the i.v. presentation of minor alloantigen-disparate spleen cells. In contrast, similar priming with cells differing solely at the H-2 major histocompatibility complex stimulated only positive T cell immunity, with no evidence of suppression. The induction of H-2 directed Ts activity could be accomplished only by i.v. priming with major plus minor incompatible donor cells, suggesting that suppressor cell recognition of minor alloantigens may have facilitated the generation of Ts against H-2-encoded major transplantation antigens. A role for minor histocompatibility antigens in the regulation of H-2-specific immunity at the effector level was also indicated. Ts induced by i.v. pretreatment with minor antigen-disparate donor cells not only suppressed the delayed-type hypersensitivity (DTH) response to the relevant minor alloantigens, but also inhibited DTH against unrelated H-2 alloantigens introduced during subsequent intradermal immunization. Suppression of H-2-directed T cell reactivity was specific in that the presence of the Ts-inducing minor alloantigens was also required and occurred only when the minor and unrelated major alloantigens were presented within the same inoculum, if not on the same cell surface. The capacity of Lyt-2+Ts or Ts-derived suppressive factors specific for one set of cell surface molecules to modulate responses to an unrelated group of surface antigens does not appear to represent a general phenomenon, because similar suppression of immunity to unrelated tumor-specific transplantation antigens by minor-specific Ts was not observed. These results are discussed with respect to the possible mechanism of H-2-directed suppression and the role of the I region in Ts recognition of antigen.

Animals↗

PubMed1984

Blocking of the response by human T-lymphocytes to extracts of autologous cancer by monoclonal antibody to Class-I major histocompatibility complex gene products in the leukocyte adherence inhibition assay.

In the leukocyte adherence inhibition (LAI) assay, about 34% of adherent T-cells from patients with breast cancer exhibit nonadherence to glass when incubated with extracts of autologous cancer but not with HLA-A, -B, and -C mismatched extracts of breast cancer. To determine whether the recognition by T-cells of tumor antigen was major histocompatibility complex restricted, major histocompatibility complex antigens in the cancer extracts or on the T-cells were coated with monoclonal antibody (MAb) to nonpolymorphic determinants. Nonadherence of T-cells was antagonized by coating the target cancer extracts with MAb to a common framework determinant of Class I HLA-A, -B, and -C antigens or to the nonpolymorphic beta 2-microglobulin, which is noncovalently associated with Class I antigens. By contrast, a MAb to a monomorphic determinant on HLA-DR antigens did not change the positive T-cell response. Moreover, coating the T-cells with MAb to HLA-A, -B, and -C did not inhibit the positive T-cell response. The positive LAI response of buffy coat peripheral blood leukocytes from patients with breast cancer to extracts of allogeneic breast cancer was not affected by coating the cancer extracts with the same MAb, indicating that MAb inhibited T-cell LAI specifically and that the antibody-dependent LAI response of buffy coat peripheral blood leukocytes was not major histocompatibility complex restricted. The results indicate that HLA-A, -B, and -C antigens in extracts of autologous breast cancer restrict the LAI response to tumor antigens of T-cells from patients with breast cancer.

Antibodies, Monoclonal↗

PubMed1980

Sensitized T-lymphocytes against paternal histocompatibility antigens cause intrauterine fetal death and growth retardation.

The influence on pregnancy of sensitized T lymphocytes against male histocompatibility antigens was investigated using inbred strain mice. Number of abortion, litter size, fetal weight and placental weight were studied on 18th day of pregnancy in the mice which were administered intravenously with T lymphocyte enriched fraction of sensitized spleen cells against allogeneic male histocompatibility antigens. The incidence of abortion in the experimental mice was higher than that in control mice. Mean fetal weight in the experimental mice was less than that in the control mice although mean placental weight in the experimental mice was unaffected. Those results show that immunologic interruption of pregnancy due to histoincompatibility between mother and fetus can occur and that the immunologic interruption of pregnancy is caused by sensitized T lymphocytes against paternal inherited histocompatibility antigens. Possible process of the immunologic interruption of pregnancy is discussed.

Animals↗

PubMed1981

Lack of histocompatibility antigens on a murine ovarian teratocarcinoma.

We have attempted to generate in vitro lymphocytes cytotoxic to a widely studied model of ovarian cancer in C3HeB/FeJ mice. These attempts were unsuccessful with either syngeneic or allogeneic spleen cells. The following experimental results demonstrated that this murine ovarian tumor lacks histocompatibility antigens. (a) Tumor cells were not lysed by allogeneic lymphocytes presensitized to H-2k spleen cells. (b) Tumor cells did not specifically inhibit the cell-mediated lysis of H-2k spleen cells by presensitized allogeneic lymphocytes. (c) Histoincompatible (H-2b or H-2d) and syngeneic (H-2k) mice all died with identical tumor growth patterns within 25, 30, or 35 days following the i.p. inoculation of 10(6), 10(5), or 10(4) tumor cells, respectively. (d) Tumor cells were not lysed by an anti-H-2k antiserum and complement. (e) Absorption of the anti-H-2k antiserum with tumor cells did not decrease the cytotoxicity of the antiserum. (f) Competitive inhibition of a radioimmunoassay and polyacrylamide gel electrophoresis of immunoprecipitate of radiolabeled tumor extracts failed to demonstrate an H-2 heavy chain, although a normal amount of beta-microglobulin was present. This lack of histocompatibility antigens may explain the failure to generate lymphocytes cytotoxic to this tumor. Thus, this murine ovarian tumor, which has a serologically detectable tumor-associated antigen and can be cured by nonspecific immunotherapy, may provide an excellent model for the study of successful immunotherapy in the absence of histocompatibility antigens and associated cell-mediated reactions.

Animals↗