Tomio Tada

Cellular interaction between cytotoxic and suppressor t cells against syngeneic tumors in the mouse.

Abstract Splenic T cells from animals bearing growing syngeneic tumors specifically inhibited the effector process of tumor cell lysis by the cytotoxic T cell which had been activated in vitro by mitomycin C treated homologous tumor. The suppression was strictly specific for the individual tumor by which suppressor cells were generated, whereas in some cases cytotoxic T cells generated by two closely related sarcomas showed a certain degree of crossreactivity. This suggests that suppressor and cytotoxic T cells recognize different antigenic moieties on tumor cells; one unique to the individual tumor and the other shared by related tumor cell lines. The suppressor T cell from tumor bearing animals possessed Ia antigen controlled by a gene in I-J subregion of H-2 major histocompatibility complex. Cytotoxic T cells generated by some but not all syngeneic tumors were also killed by anti-Ia and complement; however, the Ia antigen on such cytotoxic T cells was found to be controlled by a locus in I-A subregion. In general, the cytotoxic T cells generated by newly established tumor cell lines had Ia antigen, whereas some old cell lines, which were capable of growing across the H-2 barrier, activated the Ia negative cytotoxic T cell. These results collectively indicate that the immunological resistance against tumors is dependent on the balance of activations of the cytotoxic and suppressor T cells with different specificities and phenotypic expressions.

Suppressive and Enhancing T-cell Factors as I-region Gene Products: Properties and the Subregion Assignment

This paper describes two distinct antigen-specific T-cell factors having opposite functions in the regulation of antibody response, one suppressive and the other enhancing for a T-cell-dependent antibody response. Both factors are found to have I-region gene expressions. Available evidence indicates that they are coded for by genes present in distinct I subregions, and that the targets for these factors are probably T cells also carrying I-region determinants. Incorporating the new target cell type in the network of immunocompetent cell interactions, possible mechanisms of T-cell-mediated regulation of antibody response will be discussed.

Immunological properties of β-fructofuranosidase from ripening tomato fruit

Abstract The amount of tomato fruit β-fructofuranosidase extractable from the cell walls during ripening parallelled the changes in activity of the enzyme. Using the techniques of radioimmunoassay, double immunodiffusion analysis and immunotitration, no differences in immunological properties of β-fructofuranosidase between the various stages of fruit ripening were detected.

THE NATURE OF MASUGI NEPHRITIS HISTO- AND IMMUNOPATHOLOGICAL STUDIES*

9. Nephritogenicity of the Protein Fractions of Various Anti-Kidney Sera Masugi Nephritis Induced in Rabbits by Injections of Anti-Rabbit-Kidney Duck Serum or Gammaglobulin 1) Fundamental Pathologic Processes 2) Immunological Events Masugi Nephritis Induced in Rats by Injections of Anti-Rat-Kidney Rabbit Gammaglobulin 1 ) Fundamental Pathologic Processes 2) Immunological Events Masugi Nephritis Induced in a Rabbit by Injection of Anti-Rabbit-Kidney Guinea Pig Gammaglobulin h4asugi Nephritis Induced in Rats by Injections of Anti-Rat-Kidney Duck Gammaglobulin Masugi Nephritis Induced in Rats by Injections of Papain-Digested Anti-Rat-Kidney Rabbit Gammaglobulin Masugi Nephritis Induced in Rats by Injections of Pepsin-Digested Anti-Rat-Kidney Rabbit Gammaglobulin Masugi Nephritis Induced in Rats by Injections of Mercaptoethanol-IodoacetarnideTreated Anti-Rat-Kidney Rabbit Gammaglobulin Masugi Nephritis Induced in Rabbits by Injections of Anti-Rabbit-Kidney Duck Gammaglobulin after Preceding Sensitization with Duck Gammaglobulin, Injections of Soluble Complex of Anti-Rabbit-Kidney Duck Gammaglobulin and Anti-DuckGammaglobulin Rabbit Antibody, and Injections of both Anti-Rabbit-Kidney Duck Gammaglobulin and Anti-Duck-Gammaglobulin Rabbit Antiserum

CHARACTERIZATION OF THE ANTIGEN-SPECIFIC SUPPRESSIVE T CELL FACTOR WITH SPECIAL REFERENCE TO THE EXPRESSION OF I REGION GENES

Abstract This paper deals with the partial characterization of the antigen-specific suppressive T cell factor with special reference to its genetic nature. The suppressive T cell factor was extractable from thymocytes and spleen cells of mice that had been primed with a relatively high dose of protein antigen, and exerted a strong suppressive effect on the T cell dependent antibody response against a hapten coupled to the same carrier proteins both in in vivo and in vitro experimental systems. The factor had specificity and affinity for the immunizing antigen, but possessed no Ig determinants as revealed by absorption studies. The activity was associated with a protein having a molecular weight between 35,000 and 55,000, probably composed of small molecular weight subunits. The factor was not easily released from the primed T cell by a short-term culture with antigen. The target of the suppressive T cell factor was found to be the helper T cell with specificity for the same antigen. Absorption experiments using alloantisera against restricted subregions of the H-2 complex firmly established that the T cell factor is a product of I region genes in H-2d, H-2k and H-2S mice. Although exact location of the gene(s) codes for the T cell factor is still unknown, available evidence indicates that the factor is probably encoded by genes in the I-B (plus I-E) subregion. However, there was no correlation between the absorbing capacity and Ia specificities of alloantisera, suggesting that the factor is not an Ia molecule of known specificity. It was further found that the T cell factor can only suppress the response of H-2 histocompatible spleen cells. Studies using various combinations of strains and their F1 hybrids indicated that the acceptor site of the helper T cell for the suppressor molecule is also determined by genes on the left side half of the H-2 complex. It was postulated that paired genes in the I region code for both the suppressor molecule and acceptor site being complementary to each other.

SUPPRESSIVE T CELL FACTOR AND ITS ACCEPTOR EXPRESSED ON DIFFERENT SUBSETS OF T CELLS: A POSSIBLE AMPLIFICATION LOOP IN THE SUPPRESSOR SYSTEM*

ABSTRACT. Two functionally different subsets of T cells express determinants coded for by genes in I-J subregion. One is the producer of the suppressive T cell factor, which has the Ly 2 + ,3 + phenotype. The other is a novel cell type, which expresses the acceptor site for the T cell factor, and has Ly 1 + ,2 + ,3 + phenotype (acceptor T cell). The latter cell type is detected in a T cell population adhering to the nylon wool column, and has a high Thy 1 antigen density. The antigen-specific T cell factor, which by itself contain I region determinants acts on the latter cell type to turn it to become actual suppressor T cell. Thus the T cell factor suppresses antibody response through the intermediary of the third T cell type which perhaps participates in the final effector step of T cell-mediated suppression. The communication between the suppressor and acceptor T cells appears to be achieved via the complementary interaction of I-J subregion gene products expressed on these cell types.

Effect of Lymphocytosis-Promoting Factor of Bordetella pertussis on the Immune Response

Lymphocytosis-promoting factor (LPF) was obtained from culture filtrate of Bordetella pertussis and tested for its effect on the three well-defined cellular hypersensitivity reactio

Suppression of IgE Antibody Formation in Mice with Nonspecific Stimulation

Effects of administration of various adjuvants were examined for the induction of IgE antibody response against a hapten-carrier conjugate in the mouse. It was confirmed that alum was an excellent adjuvant for induction of IgE antibody response, while poly A:U, CFA and LPS had much less activity. However, when these adjuvants were administered before immunization with antigen and alum, they suppressed the forthcoming antibody response to various degrees. Even alum exerted a profound suppressive effect when it was given before immunization. Such suppressive effect of alum and poly A:U was partially overcome by incorporating in the adjuvant the carrier protein. In contrast the suppressive effect of CFA was overcome by incorporating in the CFA an unrelated carrier conjugated to the same hapten (DNP). The results indicate that the target of the adjuvants is different from one to the other and further give a clue to study the possible application for the suppression of IgE antibody formation.

Schistosoma japonicum: immunopathology of nephritis in Macaca fascicularis.

Abstract Macaca monkeys experimentally infected with Schistosoma japonicum developed a chronic progressive kidney lesion characterized by an increase of mesangial matrix, local glomerular hypercellularity, and local thickening of glomerular basement membrane. Immunofluorescence studies revealed the localization of IgG, IgM, IgA, and IgE immunoglobulins mostly in the mesangial area of the glomeruli accompanied by the deposition of Schistosoma antigens. By electron microscopy, in addition to the local thickening of the glomerular basement membrane, dense homogeneous deposits and those with moth-eaten appearance were detected in the mesangial matrix. These findings suggest that worms in the bloodstream continuously release antigenic materials that stimulate hosts antibody response belonging to various immunoglobulin classes including IgE. The produced antibodies and antigens would form immune complexes that deposited in the glomeruli. The increased vascular permeability caused by antigen-IgE antibody interaction may play an important role in the deposition of immune complexes and in the rapid development of kidney injury.

Revised rules for naming class I and Class II antigenic determinants controlled by the mouse H-2 complex

1 Abteilung !mmungenetik, Max-Planck-Institut ftir Biologie, Corrensstral3e 42, 7400 Ttibingen, Federal Republic of Germany 2 Department of Immunology, The Mayo Clinic, Rochester, Minnesota 3 Antoni van Leeuwenhoek-huis, Het Nederlands Kankerinstituut, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands 4 lnstitut ftir Immunologie und Genetik, Deutsches Krebsforschungszentrum, 6900 Heidelberg, Federal Republic of Germany Department of Pathology, University of Melbourne, Parkville, Victoria 3052, Australia Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 7 Immunology Branch, Transplantation Biology Section, National Institutes of Health, Bethesda, Maryland s Laboratories for immunology, School of Medicine, Chiba University, Chiba, Japan