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Poly (2'-chloro-2'-deoxyadenylic acid) and poly (2'-bromo-2'-deoxyadenylic acid) were synthesized from the corresponding diphosphates with the aid of polynucleotide phosphorylase from E. coli. UV, CD, acid titration and mixing with poly (U) were investigated. Comparing these properties with those of poly (A) and poly (2'-azido-2'-deoxyadenylic acid), it was found that 2''substituents exert significant effects on the thermal stability of these polynucleotides, though the overall conformational structure was not greatly changed.

A soluble product of macrophages (MF) and mouse viral interferon (IF) increase both major histocompatibility antigenic determinants and the number of antigen-binding cells in nonstimulated T cell-enriched mouse lymphocyte cultures. MF increases Ia and not H-2 antigens; IF increases H-2 but not Ia antigens. The increased antigen binding due to MF can be inhibited by anti-Ia but not by anti-H-2 sera, whereas IF-induced binding is sensitive to anti-H-2 but not to anti-Ia sera. The specificity of IF- or MF-induced binding of branched synthetic polypeptides by T cells is different from that of B cells and similar to the specificity of the Ir gene regulation. MF increases antigen binding only in Ir high-responder animals. The IF-induced antigen binding is not dependent on the Ir genotype. MF-reactive cells express the Ly-1 marker, and the IF-reactive antigen binders express the Ly-2 phenotype. It is suggested that MF and IF are physiological mediators of antigen binding by T cells.

Sequential immunoprecipitation analyses of Ia antigens were performed with 125I-labeled B10, B10.A(3R), and B10.A(5R) spleen cell lysates. The results suggest the presence of one I-region associated (Ia) locus (Ia-1) in the I-A subregion. In addition, they indicate that two Ia loci map between the I-J and S regions. One locus, Ia-5, maps in the I-E subregion. The second locus, most likely Ia-3, maps in either the I-E or I-C subregion. Taken together, the data demonstrate that at least three Ia loci in the I-region of the H-2 complex code for molecules detectable by immunoprecipitation.

Diabetes in idiopathic hemochromatosis has been considered to be secondary to islet cell damage resulting from the iron deposits. Plasma glucagon was measured by immunoassay using the pancreas specific 30-K antiserum, and was found to be normal or slightly elevated during arginine-infusion tests in patients exhibiting both hemochromatosis and pathological glucose tolerance. This suggests that diabetes in hemochromatosis is not due to a lesion resulting from the iron deposits. The two affections appear to be merely associated and are possibly genetically linked.