Many sera from normal individuals as well as patients with various disease states contain agglutinating antibodies which show specificity for antigenic determinants of γ-globulin revealed by pepsin digestion at pH 4.1. Sera containing such agglutinating activity as well as sera negative for these agglutinators contain low molecular weight (3S–5S) components of slow γ-mobility which inhibit these agglutination reactions. Low molecular weight inhibitors show both auto- and isospecificity, and are antigenically related to the 5S pepsin fragment of γ-globulin. A common situation is thereby revealed in which human anti-γ-globulin antibodies showing specificity for pepsin-digested γ-globulins are present in serum along with low molecular weight γ-globulin components capable of inhibition. Autoreactivity or autospecificity of such anti-γ-globulin factors is a phenomenon shared by both normal human sera and sera from patients with various disease states.
Encephalomyocarditis virus (EMC) is a member of the picornavirus group. Oral infection of mice produces viremia and fecal virus excretion which are followed by fatal encephalitis. EMC is similar to poliovirus physically and chemically, and Friedman and Maenza have suggested that EMC infection in mice be used as a model of poliovirus infection (1).Oral attenuated virus vaccine prevents the subsequent infection of the bowel with a homotypic virulent challenge in both EMC (1) and poliovirus ( 2 ) infection. Parenteral inactivated vaccine does not convey firm protection against infection of the bowel with poliovirus ( 3 ) , and antibody to poliovirus is found in duodenal secretory gamma A immunoglobulin after oral attenuated virus but not after parenteral inactivated virus (4).Because of interest in the influence of the route of immunization on the subsequent resistance of the gut to infection, we have compared the effect of oral living-attenuated EMC with the effect of subcutaneous formalin-inactivated EMC on fecal excretion of virus following an oral virulent challenge.Materials and Methods. In general, the procedures used by Friedman and Maenza were followed (1). Virus was grown in L-cell monolayers maintained in Eagle's basal medium containing 20% fetal bovine serum, and virus titers were determined by plaque formation (1). A virulent and an attenuated strain of the virus were used. Both were kind-
Summary
Digestion of γ-chains by trypsin, chymotrypsin, and bacterial protease produced a spectrum of changes in antigenic determinants revealed by the fine specificity of human rheumatoid factors as sources of 19S antibody to human IgG. Gm(a) activity was greatly reduced by chymotrypsin and bacterial protease digestion of γ-chains. Trypsin digests of γ-chains retained inhibitory capacity for both Gm(a) and Gm(b1) systems. By contrast, changes produced by reduction in 4 to 8 M urea did not destroy Gm(a) activity, but abolished Gm(b1) activity. These findings were amplified by digestion and urea reduction of γ-chains from Gm(a)+ and Gm(b1) + myeloma proteins.
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