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E Gomard

Publications and source records attributed to E Gomard.

At least 73 records · Page 4Linked to original sources
PubMed1981

[Localization, in the D region of the major histocompatibility complex, of the genes controlling the level of killer T-cell mediated antiviral response through the phenomenon of restriction by H-2 antigens].

In two different murine systems it is shown that immune response genes, mapping to the D region of the major histocompatibility complex, control the level of the immune response mediated by cytolytic T lymphocytes and specific for the virus induced FMR antigens. The high responder phenotype is dominant. It is associated with the choice of certain H-2 antigens as restricting factors of the T lymphocyte activity, histocompatibility antigens behaving like Ir gene products.

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PubMed1981

Accessory cells in the in vitro generation of type C virus-specific T killer lymphocytes. II. Demonstration of a T helper cell in the spleen of in vivo primed mice.

The existence of a helper T cell cooperating with cytolytic T lymphocytes (CTL) in cell-mediated anti-tumor responses specific for the virus-induced FMR antigens can be demonstrated by using unprimed thymocytes as CTL precursors and in vivo primed irradiated spleen cells as helper. The helper T cells express Thy-1.2 and Lyt-1.2 antigens at their surface, but not Lyt-2.2. The helper function required the presence of macrophages to be detected, is antigen specific, and appears unusually radiosensitive compared with previously described helper T cell function.

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PubMed1981

Accessory cells in the in vitro generation of type C viruses specific T killer lymphocytes. I. Role of macrophages in primary anti-FMR reaction.

The role of macrophages has been studied in in vitro cytolytic T lymphocytes- (CTL) mediated responses directed against the FMR cell-surface antigens induced by C type viruses. Macrophages, defined as Thy 1.2-negative, Ia-positive, adherent, phagocytic, radioresistant cells present in the spleen and the peritoneal cavity, are required to obtain primary in vitro anti-FMR responses. In most of our experiments they were not necessary in secondary reactions. In primary responses, macrophages and responder T cells must be compatible at least at the I region of the major histocompatibility complex. Anti-Ia antibodies inhibit the response. A rat soluble factor (Interleukin 2) can replace macrophages in primary anti-FMR CTL-mediated reactions. These results suggest that macrophages function during primary anti-FMR response by interacting with a helper T cell rather than with CTL precursors. In agreement with this hypothesis, it appears that the H-2 restriction of F1 hybrid anti-FMR CTL generated in vitro in primary reaction is not related to the H-2 specificities of the parental macrophages used and depends only on the H-2 antigens of the stimulating tumor cells.

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PubMed1980

Immune response genes control T killer cell response against Moloney tumor antigen cytolysis regulating reactions against the best available H-2 + viral antigen association.

Cytolytic T lymphocytes (CTL) specific for the virus-induced and leukemia-associated Friend, Moloney, Rauscher (FMR) antigen are easily detected in the spleens of primary and secondary stimulated H-2b or H-2d mice. They react, respectively, with H-2Db + FMR and H-2Kd + FMR; Dd and Kb never being involved. On the other hand, recombinant (KbDd) mice are relatively low responders that produce CTL only after secondary stimulation. Competition and blocking experiments with monospecific anti-H-2 antibodies have demonstrated that on the same H-2b tumor cells, C57BL/6 (H-2b) lymphocytes recognize Db + FMR, whereas B10.A(5R) lymphocytes recognize Kb + FMR, the restriction cannot, therefore be explained by a specific association of viral molecules with certain H-2 products. The CTL response of (B10 X 5R)F1 hybrids is (a) easily detected in primary reaction, the high responder anti-FMR phenotype being dominant and (b) directed against Db + FMR, F1 mice being low responder against Kb + FMR like the B10 parent. These results suggest that a D region-associated immune response gene controls the cell-mediated anti-FMR reaction, the best available H-2 + FMR antigenic association being chosen by CTL precursors.

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PubMed1979

Significance of the proline assay in the study of anti-MSV cell-mediated immune reactions.

The cytolysis of 3H-proline-labelled tumour cells growing in monolayer by syngeneic immune lymphocytes has been studied in the murine sarcoma virus (MSV) system. Results show that the proline assay (PA) is a convenient way to reveal the activity of cytolytic T lymphocytes against FMR-like antigens. Using the same effector and target cells, the classical chromium-release test (CRT) fails to reveal any cytolytic activity, and the visual microcytotoxicity assay as well as several derived isotopic methods are known to reveal mainly non-specific reactions due to non-T effector cells. The PA, therefore, appears to be a useful method for testing an antitumour reaction against tumour cells in monolayer. The results are, however, different from those obtained in the CRT using the same effector cells but lymphoma cells in suspension as targets, the major discrepancies being the following: (a) the PA does not provide truly quantitative data, due to the very high lymphoid: effector cell ratios needed in this test; (b) unexpected patterns of antigenic specificities are sometimes detected in PA; (c) a non-specific natural killer activity of non-T cells is frequently detected in the PA, masking at low lymphoid: target cell ratios the T-dependent specific cytolysis; (d) the H-2 restriction of the cytolytic T-cell activity is poorly detected in PA, whereas the role of H-2 antigens is clearly shown by blocking experiments using anti-H-2 antibodies.

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PubMed1977

Exclusive involvement of H-2Db or H-2Kd product in the interaction between T-killer lymphocytes and syngeneic H-2b or H-2d viral lymphomas.

It was demonstrated previously that the cytolysis of murine viral lymphoma cells by anti-murine sarcoma virus (MSV) syngeneic T-killer lymphocytes was restricted by some products of the H-2 complex. The respective role of the products of different regions of the H-2 complex were studied with six H-2(b) and three H-2(d) lymphomas induced by five different type C viruses. They were tested in a classical chromium release test against anti-MSV T-killer cells obtained from different inbred strains of mice, including several H-2 recombinants. Tumors o pound the H-2(b) haplotype were lysed only when effectors and target cells have in common the D(b) region. On the contrary an identity limited to the K end of the H-2 complex is necessary and sufficient in the H-2(d) haplotype. An in vitro restimulation of the spleen cells with concanavalin A strongly increased the activity of in vivo-primed T lymphocytes but did not provide any response for in vivo-primed but nonresponder cells. Preincubation of the tumor cells with anti-H-2 sera abolished the lysis by syngeneic anti-MSV effector lymphocytes. The same results were obtained by preincubating the H-2(b) targets with anti-H-2D(b), or the H-2(d) target with anti-H-2K(d). Preincubation with anti-H-2K(b) or anti- H-2D(d) were ineffective. These results show that the T-killer/target cells interaction in the MSV system involved some products of the H-2 complex which might be different with the various H-2 haplotypes and could possibly vary according to the antigenic specificity. A specific association of a viral product with a normal cellular structure, directed by the H-2 region during the viral budding could explain the observed results.

Animals↗
PubMed1977

Relationships between H-2 and viral antigens in murine oncornavirus-induced tumours.

Cytolytic T lymphocytes (CTL) from murine sarcoma virus (MSV) or Friend leukaemia virus (FLV) inoculated mice lyse syngeneic much more efficiently than allogeneic FMRGi+ lymphoma cells. By comparing the cytolysis of various H-2 different 51Cr lymphomas by CTL from several inbred and congenic lines differing at H-2, and by competition experiments using unlabelled cells, one can demonstrate that this phenomenon is due to an H-2 barrier. H-2b/H-2d hybrid-anti-MSV-CTL immunized by H-2b, H-2d or H-2b/H-2d tumours lyse only FMRGi+ lymphomas of the same H-2, and their activity for a given target is inhibited only by H-2-identical competitive cells. H-2 antigens are therefore directly involved in the interaction between tumour cells and immune CTL which probably react with an 'H-2 modified' antigen of the tumour cells surface. The use of CTL from intra-H-2 recombinant lines shows that H-2D and probably H-2K molecules are involved, but vary according to the tumour cells. A possible role of the I region is discussed as well as the implications of these results in immunosurveillance against viral neoplasia.

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