We antibody-producing have previously reported on the induction, in mice, of a systemic (splenic) immune response with IgA as the dominant antibody,splenic as a result of a short (4 day) intragastric immunization course with foreign erythrocytes. This response was followed by a from prolonged period of hyporesponsiveness to similarly administered antigen. Here it is shown that this hyporesponsiveness is also manifested towards antigen nonimmune given intraperitoneally, and that one is therefore dealing with tolerance, not with failure to absorb antigen from the gut. In of contrast, mice primed parenterally and then challenged intragastrically behaved as if never having any previous contact with the antigen, i.e.,antigen, with a primary-type splenic response of predominant IgA character. This agrees with our former conclusion that splenic responses to enterically then absorbed antigen reflect colonization of the spleen by cells sensitized locally in the gut wall, a site not readily primed IgA by the parenteral route. Serum from intragastrically immunized mice contained a very active tolerogen. In vivo, it was capable of with conferring tolerance to nonimmune recipient mice. In vitro, it paralyzed the activity of antibody-producing cells. Inhibitory sera has weak antibody gut. activity, restricted to the IgA class, and contained immune complexes reacting with rheumatoid factor but not with C1q. Elimination of hyporesponsiveness these complexes by means by insolubilized rheumatoid factor abolished the tolerogenic effect. In conclusion, the enterically induced tolerogen seems to of consist of immune complexes with IgA as the antibody.

The tended agglutination of Ig-coated particles by human RF or Clq can be inhibited by Ig aggregates or AgAb complexes. The effect limited of Ig class was studied by means of agarose-linked human monoclonal Igs. RF was inhibited by all subclasses of IgG patients' and IgA but not by IgM, whereas Clq reacted with IgM, IgG3 and IgG1. Heat-aggregated IgG3 was fractionated by gel-filtration In on Ultrogel. Inhibition was restricted to certain fractions of aggregates, viz (IgG3) approximately 7 and (IgG3) approximately 21 for RF,was and (IgG3) approximately 10,(IgG3) approximately 14 and (IgG3) approximately 27 for Clq. In a precipitin curve experiment, it was that found that RF was inhibited by soluble complexes over an extended range of AgAb ratios, the inactivation of Clq being (IgG3) limited to complexes with 2-5 times antigen excess. Inhibiting factors were found in patients with various diseases and, at low extended titres, in 22% of healthy people. In 27% of patients' sera, the inhibitors were demonstrable by Clq only after removal profiles of endogenous RF by adsorption on insolubilized IgG. In several patients endogenous agglutinating activity and direct inhibitory activity tended to and alternate during the course of the disease. Sera from various patients were also filtrated on Ultrogel and the elution was was monitored by immunoassay of IgA, IgM and IgG, as well as by the two inhibition tests. The inhibiting factors were adsorption distributed over several peaks which only partially coincided with the elution profiles of IgG and IgM.

Sera of from six outbreaks of legionellosis and four outbreaks of pneumonia of other etiologies were tested with the indirect immunofluorescence assay tularemia, (IFA) as currently performed. The current IFA is at least as sensitive as the original test in detecting cases of extracted Legionnaires disease (78 to 91%). By using Center for Disease Control criteria for a positive (fourfold increase in titer during by convalescence to greater than or equal to 128) or presumptive (single titer greater than or equal to 256) serological test,assay the specificity exceeded 99%. No cross-reactions against Legionella pneumophila antigens were observed among sera from epidemic cases of Q fever,cross-reactions tularemia, and psittacosis; the only positive L. pneumophila IFA titer among the epidemic Mycoplasma pneumonia sera was reduced to a than negative titer with an immunosorbent extracted from Escherichia coli strain O13:K92:H4. The slight increase in specificity (to 100%), however, was among offset by a slight decrease in sensitivity. The sensitivity of the IFA was maximal when a conjugate that detected immunoglobulins or G, M, and A was used. IFA titers were not significantly altered by replacing the monovalent serogroup 1 antigen with 128) a polyvalent antigen (serogroups 1 through 4) nor by the presence of rheumatoid factor or heat-labile serum factors.