Alternative Routes of Entry for Cell Surface Antigens Into the Immune System

Clark, Edward C.; Lake, Phil; Mitchison, N A; Nakashima, Izumi

doi:10.1016/b978-0-12-584650-9.50024-9

Natural and Induced Cell-Mediated Cytotoxicity 1979

DOI: 10.1016/b978-0-12-584650-9.50024-9

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Alternative Routes of Entry for Cell Surface Antigens Into the Immune System

Edward C. Clark¹,

Phil Lake²,

N A Mitchison³

et al.

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1982

1983

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Immune recognition of tumor cells in vivo. I. Role of H‐2 gene products in T lymphocyte activation against minor histocompatibility antigens displayed by adenocarcinoma cells

et al. 1982

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Challenges from ADK-1t adenocarcinoma cells of BALB/c (H-2d, Mlsb) mouse origin are rejected by DBA/2 (H-2d, Mlsa) mice on the basis of differences in a limited number of minor histocompatibility antigens. This T lymphocyte-dependent reaction is highly specific, and efficiently triggered only by Ia+ leukocytes infiltrating the tumor mass. ADK-1t challenges depleted of Ia+ infiltrating BALB/c leukocytes grow and kill DBA/2 mice, whereas the simultaneous injection of Ia+-inactivated BALB/c leukocytes induces tumor rejection. The expression of Mlsb-incompatible determinants on the Ia+ BALB/c leukocyte membrane is irrelevant in the induction of this efficient T lymphocyte reaction against BALB/c minor histocompatibility antigens. By contrast, a critical requirement is H-2 matching between the Ia+ leukocytes and the recipient mice at the inductive phase of the reaction.

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Immune recognition of tumor cells in vivo. I. Role of H‐2 gene products in T lymphocyte activation against minor histocompatibility antigens displayed by adenocarcinoma cells

et al. 1982

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ROUS SARCOMA VIRUS‐INDUCED TUMOURS IN MICE: II. CONTRIBUTION OF H‐2 AND NON‐H‐2 ALLOANTIGEN BARRIERS TO TUMOUR IMMUNOGENICITY IN VIVO

Forni

Giovarelli

Sarzotti

et al. 1983

Int J Immunogenetics

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SUMMARY The features of the immune recognition of a murine fibrosarcoma induced by Rous sarcoma virus were tested in histocompatible and histoincompatible mice. No evidence of a genetic regulation of spontaneous reactivity to tumour‐associated antigens was found in various histocompatible F1 hybrids. Incompatibility in multiple minor histocompatibility antigens triggers a host reaction incapable of causing tumour rejection in some cases. The growth rate of incipient tumours is unaffected, whereas that of already visible tumoour masses is significantly delayed. Admixture to the challenge of inactivated leukocytes bearing the same minor histocompatibility antigens as the tumour triggers a significantly stronger reaction. The reaction of hosts incompatible in the H‐2K or H‐2DL regions is quite efficient. However, the intensity of the immune reaction to H‐2DLs antigens displayed by tumour cells is markedly dependent on the alleles of genes located in the central regions of the H‐2 complex.

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Alternative Routes of Entry for Cell Surface Antigens Into the Immune System

Cited by 2 publications

References 0 publications

Immune recognition of tumor cells in vivo. I. Role of H‐2 gene products in T lymphocyte activation against minor histocompatibility antigens displayed by adenocarcinoma cells

Immune recognition of tumor cells in vivo. I. Role of H‐2 gene products in T lymphocyte activation against minor histocompatibility antigens displayed by adenocarcinoma cells

ROUS SARCOMA VIRUS‐INDUCED TUMOURS IN MICE: II. CONTRIBUTION OF H‐2 AND NON‐H‐2 ALLOANTIGEN BARRIERS TO TUMOUR IMMUNOGENICITY IN VIVO

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