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E Kölsch

Publications and source records attributed to E Kölsch.

At least 91 records · Page 5Linked to original sources

Genetic control of the immune response to phage fd. IV. Complementation between H-2-linked Ir genes.

The immune response to bacteriophage fd has been tested in congenic resistant strains of mice. B10 mice are high responders; B10.BR and B10.D2 mice are low responders. B10.A mice with the recombinant H-2a haplotype as well as heterozygous H-2k/d (B10.BR X B10.D2) F1 mice respond with high antibody titers, indicating the existence of two complementing Ir genes. From the results obtained with recombinant and F1 hybrid mice, Irfdalpha can be localized to the right of the crossover between the IE and IC subregions, Irfdbeta to the left of IB, presumably at IA. Complementation is observed with selected pairs of alleles only, suggesting alpha-beta coupled complementation. In addition to genes in the H-2 complex, there are non-H-2 background genes modulating H-2 regulated anti-fd response. B10.BR mice lack primary IgM and IgG antibodies, yet are able to mount a secondary IgG anti-fd response, giving evidence for intact memory formation in this low responder strain. The combined data are most easily interpreted by assuming that both H- and non-H- genes modulate the effective immunogenic dose of antigen.

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Influence of different antigen doses on number and properties of antigen binding cells.

The number of antigen binding cells, as revealed by capping experiments, is strongly influenced by the concentration of antigen used. At high concentrations of antigen an additional population of cells of the size of lymphocytes can be detected, which is not stained after incubation with low doses of antigen. These cells bear immunoglobulin on their surface and can be removed from the spleen by carbonyl iron treatment.

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The genetic control of T cell-mediated immunity against the DBA/2 mastocytoma P-815. II. Low responsiveness in T cell-mediated cytotoxicity accompanied by the inability to produce antibodies in a secondary response.

Low responsiveness of DBA/1 mice in T cell-mediated cytotoxicity against the DBA/2 mastocytoma P-815 (H-2d) is genetically controlled and inherited as a recessive trait. For an analysis of the humoral anti-H-2d response of DBA/1 mice after immunization with P-815 mastocytoma cells both complement-dependent lysis (CDL) and the cytotoxicity inhibition assay (CIA) were used to demonstrate antibodies. Both assays show that DBA/1 mice are unable to produce anti-H-2d antibodies in a secondary response. Even high doses of immunizing cells give only a weak response. The response is fully recovered upon allogeneic interaction. A transient primary anti-H-2d activity can be found in the CIA but not by CDL. The data show that the genetically controlled determinant-specific defect in T cell-mediated cytotoxicity among DBA/1 mice has its correlate in a blockade of memory formation or expression in the humoral anti-H-2d response.

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Correlation of "sneaking through" of tumor cells with specific immunological impairment of the host.

The preferential take of tumors after small-size inocula of transplantable tumor cells has been described for many systems. The phenomenon has been named "sneaking through" or "dilution escape". Using a BALB/c mastocytoma, we have analyzed the immunological parameters accompanying sneaking through that can be observed upon injection of 10(1) to 10(3) living cells. Mice can also be conditioned by injection of low, subimmunogenic numbers of irradiated cells to show increased tumor incidences upon injection of living cells in doses two orders of magnitude above the sneaking through dose. The general immune reactivity of the animals is not impaired under these conditions. However, determinant-specific unresponsiveness is found which can be transferred by spleen cells and therefore seems to be actively maintained. It is concluded that sneaking through of tumor cells is the result of specific immunological impairment of the host's immune system by subimmunogenic small-size inocula of tumor cells.

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The subcellular distribution of antigen in macrophages.

The intracellular fate of phagocytosed antigens in cells from peritoneal exudate in CBA mice has been studied by using (126)I and (131)I labeled antigens. After uptake of labeled antigen, cells were homogenized and the subcellular fractions were analyzed by isopycnic centrifugation in a sucrose gradient. The uptake of heat-denatured BSA (c BSA) by these cells in vivo is 3.5 microg/mg c BSA injected/10(8) cells. The uptake by cells in animals which were exposed 2 days earlier to 900 r whole body irradiation is slightly lower but does not differ significantly. 90% of the phagocytosed material is degraded within 2-3 hr, the residual 10% is retained at least over an 8 hr periods. Using a pulse and chase technique, with (125)I and (131)I c BSA in vitro and in vivo it was shown that newly phagocytosed antigen is found mainly in a lysosomal turnover compartment of a density 1.19 g cm(-3). Antigen which has been in the cells for longer was found in a denser fraction (1.26 g cm(-3)). In a comparison of nhrmal and X-irradiated cells it can be shown that after irradiation with 900 r less c BSA is found in this storage compartment. Binding of the antigen to the subcellular fractions, and its behavior towards several detergents has been studied. Subcellular fractions do not have the increased immunogenic capacity of antigen enclosed in living macrophages. Two synthetic polypeptide antigens, poly(D-Tyr, D-Glu, D-Ala) and poly-(L-Tyr, L-Glu) have a different subcellular distribution from c BSA, BSA, or bovine gamma globulin. Apart from also being found in the 1.26 storage compartment the polypeptide antigens are mainly located in a 1.15 compartment and only to a small extent in the 1.19 compartment. The half-life of these antigens in the cells is much longer than the half-life of the protein antigens studied. The finding of several subcellular compartments is discussed in connection with the functions possibly performed by macrophages.

Acid Phosphatase↗