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A chemically induced sarcoma of BALB/c (H-2d) mice, MCG4, is shown to induce in BALB/c lymphocytes a primary anti-tumor cytolytic T lymphocyte (CTL) reaction in vitro. The anti-tumor CTL showed tumor specificity but reacted also with normal cells expressing distinct H-2 alloantigens. The CTL response could be shown to be induced by and directed against alloantigenic determinants expressed on two different molecules, one H-2Kk-like the other H-2Dk-like. The biological significance of these findings is discussed with regard to (i) possibility of derepression of normally silent H-2 genes in tumor cells and normal cells, (ii) generation of alloreactivity in ontogeny, and (iii) role of alloreactive T cells in eliminating cells expressing wrong gH-2 antigens.

Loci clustered in the I region of the murine H-2 gene complex control the capacity to generate an immune response against foreign antigens (Ir loci) and control differentiation antigens which appear to serve as structures used by cells to interact with and regulate one another (Ia loci). Both genetic and functional studies suggest that Ia antigens may be products of Ir loci. Recent studies have shown that interaction between closely linked Ir loci is required for generating immune responses to certain foreign antigens, and that interaction between H-2-linked loci determines the appearance of an Ia glycoprotein (the Ae chain) on lymphocyte cell surfaces. In this report, we show that one Ia locus regulates the quantitative expression of the product (the E alpha chain) of a second Ia locus. This regulatory locus is dominantly expressed and exerts its effects in either the cis or trans chromosomal position. Thus, the quantitative as well as the qualitative expression of some Ia products is dependent on interaction between tightly linked loci. Our results suggest a possible molecular basis for this regulation: the synthesis and intracellular association of Ae and E alpha chains may be an absolute requirement for the expression of normal levels of either polypeptide chain on the lymphocyte cell surface. The implications these findings have for I region control of immune responses and study of human HLA-D antigens are discussed.

The field of coagulation testing has undergone some major technological and conceptual developments, which are briefly reviewed here. The assessment of coagulation parameters is no longer restricted to the study of clot formation and its dissolution. The understanding of the biochemical nature of coagulation processes, coupled with the development of new therapeutic agents in the treatment of hemostatic disorders, has brought about the development of fast, reliable, and clearly defined laboratory test procedures to evaluate the components of this system. The introduction of methods involving synthetic substrates has been very significant because many of the coagulation parameters can now be measured with a spectrophotometer or fluorometer, by methods that lend themselves to the automation found in most large clinical chemistry laboratories. In our laboratory, we use automated synthetic-substrate methods for antithrombin-III, plasminogen, and prothrombin, and are developing the synthetic-substrate assay equivalent of clot-based prothrombin time and partial thromboplastin. Immunological methods such as laser/rate nephelometry, enzyme-linked immunoassays, electroimmunodiffusion, and radioimmunoassays have been utilized to evaluate coagulation proteins. The relation of functional and immunological properties of these proteins to their physiological function is being studied. In coming years the testing of coagulation function will undergo some major changes and will require input from clinical chemists and other laboratory scientists to facilitate the technology transfer and proper standardization of new methods.

Interaction of estradiol and testosterone was studied at the level of cytoplasmic and nuclear estrogen receptors in the uterus of the adult rat. 55 Sprague-Dawley strain rats, 10 weeks old, were divided into 4 groups. Group I. 5 intact rats (proestrus). Group II. 30 rats were injected with long acting estradiol (ED: 1mg/0.2ml of estradiol dipropionate). Each 5 rats were sacrificed on day 1, 3, 5, 7, 11 and 14 days respectively after the ED injection. Group III. 10 rats were injected with ED. Vehicle (0.2ml of dimethyl sulfoxide) and 1mg/ 0.2ml of testosterone were injected from the 3rd day of the ED injection for 5 days into each 5 rats respectively. Group IV. 10 rats were injected with ED. The rats were treated similarly to Group III except that vehicle or testosterone injections began from the 7th day. Plasma estradiol was determined by RIA. The DCC method for cytoplasmic receptor assay and the pellet exchange method for nuclear receptor assay were used. As to unbound receptor assay, the material was incubated with tritiated estradiol at 0 degrees C for 2 hours. Incubation at 30 degrees C for 1 hour was added to the above for bound receptor assay. Plasma estradiol levels increased 1 day after the ED injection and remained very high for 7 days and decreased to five times that of intact rats 14 days after the injection. Plasma estradiol levels were not influenced by injections of vehicle or testosterone. In group II, cytoplasmic estrogen receptor decreased 1 day after the ED injection and remained low for 7 days and then returned gradually. In nucleus bound receptor increased. Fluctuation of estrogen receptors in uterine cytoplasma and nucleus was in accordance with the concentration of plasma estradiol. In Groups III and IV, there was no significant difference in cytoplasmic and nuclear estrogen receptors between vehicle and testosterone injections. Plasma estradiol levels and uterine cytoplasmic and nuclear estrogen receptors of the ED-treated rats were not influenced by testosterone injections. It is supposed that interaction of estradiol and testosterone may occur in the protein or DNA synthesis mechanism after the receptor level.