GENETIC CONTROL OF IMMUNE RESPONSES IN VITRO : V. STIMULATION OF SUPPRESSOR T CELLS IN NONRESPONDER MICE BY THE TERPOLYMERL-GLUTAMIC ACID60-L-ALANINE30-L-TYROSINE10 (GAT)

In recent studies we have found that GAT not only fails to elicit a GAT-specific response in nonresponder mice but also specifically decreases the ability of nonresponder mice to develop a GAT-specific PFC response to a subsequent challenge with GAT bound to the immunogenic carrier, MBSA. Studies presented in this paper demonstrate that B cells from nonresponder, DBA/1 mice rendered unresponsive by GAT in vivo can respond in vitro to GAT-MBSA if exogenous, carrier-primed T cells are added to the cultures. The unresponsiveness was shown to be the result of impaired carrier-specific helper T-cell function in the spleen cells of GAT-primed mice. Spleen cells from GAT-primed mice specifically suppressed the GAT-specific PFC response of spleen cells from normal DBA/1 mice incubated with GAT-MBSA. This suppression was prevented by pretreatment of GAT-primed spleen cells with anti-θ serum plus C or X irradiation. Identification of the suppressor cells as T cells was confirmed by the demonstration that suppressor cells were confined to the fraction of the column-purified lymphocytes which contained θ-positive cells and a few non-Ig-bearing cells. The significance of these data to our understanding of Ir-gene regulation of the immune response is discussed

Strategies to increase austenite FCC relative phase stability in high-Mn steels

Several strategies to increase the FCC austenite stability compared to BCC and HCP martensites have been tested and are discussed. The relative stability of the different phases was analyzed by studying the effects of: a) grain size, b) antiferromagnetic ordering of the austenite, c) thermal cycling through the FCC-HCP transition, d) plastic deformation of the austenite and e) combined effects. As a first step, the effect of decreasing the grain size was analyzed in Fe-Mn alloys for Mn contents smaller than 18 wt.%, where BCC and HCP martensites compete in stability. Formation of the BCC phase is inhibited for 15 wt.% and 17 wt.% of Mn for grain sizes smaller than 2 μm. This enabled, for the first time at these compositions, the measurement of the Neel temperature of the austenite using specific heat and magnetic measurements. A comparison of the obtained transition temperatures with accepted models is discussed. The effect of modifying the grain size on the FCC-HCP transition temperatures was also analyzed for 15 wt.% and 17 wt.% Mn contents showing a complete HCP inhibition for grain sizes smaller than 200 nm. A nucleation model for the HCP martensite is considered which includes an additional resistance to the transformation term depending on the austenitic grain size. Additional combined effects on the FCC stabilization are discussed like the interaction between the antiferromagnetic ordering and the introduction of defects by thermal cycling through the martensitic transformation. The analysis can be easily applied to systems with a larger number of components. Results obtained in the Fe-Mn-Cr system are also presented.The authors acknowledge the financial support from ANPCyT (PICT-2017-2198), CONICET (PIP 2015-112-201501-00521), CONICET (PIP 2017e2019 GI 0634), ANPCyT (PICT-2017-4518), and Universidad Nacional de Cuyo (06/C516 and 06/C588)

IMMUNE RESPONSES IN VITRO : XI. Suppression of Primary IgM and IgG Plaque-Forming Cell Responses In Vitro by Alloantisera Against Leukocyte Alloantigens

The effects of alloantisera against leukocyte alloantigens on plaque-forming cell (PFC) responses to sheep erythrocytes and the terpolymer of L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT) by mouse spleen cells in vitro have been investigated. Polyspecific antibodies against both H-2 and non-H-2 alloantigens on responding spleen cells suppressed both IgM and IgG PFC responses; antisera against alloantigens coded for by the K and I regions, but not the D region, of the H-2 complex also effectively suppressed PFC responses. The suppression was not due to cytotoxicity to the spleen cells or anti-immunoglobulin activity in the sera and was directly related to the amount of antiserum added to the cultures. The suppression was specific for spleen cells against which the alloantiserum was directed. The alloantisera suppressed responses most effectively when present during the first 24 h of incubation, and although not rendering lymphoid cells incapable of developing PFC responses after removal of noncell-bound antibody, did act by interfering with successful initiation of the PFC response. The alloantisera suppressed both IgM and IgG PFC responses when directed against alloantigens only on macrophages, but selectively suppressed IgG responses when directed against alloantigens only on lymphoid cells. The alloantisera did not interfere with the ability of macrophages to bind GAT or to support the viability of the lymphoid cells, but did interfere with the ability of macrophage-associated antigen to effectively stimulate antibody responses by the lymphoid cells. Possible mechanisms for the effects of alloantisera on macrophages and the selective suppression of IgG responses when the antisera are directed against alloantigens on lymphoid cells are discussed with reference to our current understanding of genetic restrictions governing cell interactions in the development of antibody responses in mice