Differentiation of pemphigus antibodies of the vulgaris and follaceus types on monkey and guinea pig esophagus sections.
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Biomedical subjects
Publications and source records attributed to S A Krasny.
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We report here direct immunofluorescence studies of normal skin biopsies that exhibited only complement C3 staining in intercellular areas of epithelium with a view toward evaluating the significance of such findings. During a 5-year period, 11,000 skin biopsy specimens were examined for in vivo binding of immunoglobulins, fibrin, and complement C3 by means of defined direct immunofluorescence methods. Four of ten patients demonstrating intercellular C3 deposits alone had drug-related reactions or erythema multiforme, and four were subsequently shown to have a connective tissue disease. Pemphigus was ruled out in all ten cases in these retrospective studies. These observations indicate that the finding of intercellular C3 deposits in the absence of IgG in normal skin is not a sign of pemphigus but, rather, a sign either of an unusual type of drug reaction or, possibly, of some connective tissue disease. However, the finding of intercellular C3 plus IgG (with or without other immunoglobulins) is a sign of pemphigus. The mechanism of C3 deposition without immunoglobulins is not clear.
Our immunologic studies of twenty-five patients with acrosclerosis with severe acral involvement, twenty-seven patients with most or all of the signs of CREST syndrome, twenty-two patients with systemic lupus erythematosus as positive controls, and ninety-one blood donors as negative controls centered on an evaluation of eight antigenic substrates, including four types of human cells for the detection of anticentromere antibodies (ACA) and other antinuclear antibodies (ANA). The ACA, which occurred only among the patients with most or all of the signs of CREST syndrome, could be detected reliably on human cell lines HEp-2 and KB but not on a mouse cell line or on the three types of tissue sections examined. Comparisons of human HEp-2 and KB cell lines from four sources indicated that HEp-2 cells are the best of the substrates tested for detection of ACA. Since rodent tissue sections give negative reactions with ACA, they are indicated for confirmation. In general, results varied with the type and source of antigen used. Thus ANA findings need to be expressed not only in terms of the titers of the antibodies and the pattern(s) of their reactions but also in terms of the type of antigen or substrate used, its source, and the diagnostic significance of findings in the given test system.
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Livers, sera, and erythrocytes of MAXX, BN, and Wistar rats were examined for an antigen (CRA) that cross-reacts with enterobacterial common antigen (ECA). Extracts of these tissues were tested for their capacity to reduce anti-ECA titers. By this parameter, CRA was present in certain, although not all, extracts of rat tissue. None of the extracts modified red blood cells (RBC) for agglutination by anti-ECA antisera, nor did MAXX liver extracts engender anti-ECA activity in rabbits. It was speculated that a repressor is present in rat tissue that affects both antigenicity and immunogenicity of CRA. To test this concept, extracts of mixtures of enterobacterial suspensions and liver homogenates were prepared. ECA in the presence of tissue did not modify RBC for anti-ECA activity as did ECA alone, nor did enterobacteria-liver extracts significantly reduce anti-ECA titers. Administration of ethanol-soluble fractions of enterobacteria-liver mixtures to rabbits did not elicit an anti-ECA antibody response as did ECA alone. The finding of CRA in certain rat tissues, sera, and erythrocytes may account, in part, for rats being refractory to immunization with ECA. It is proposed that repressors may mask or abrogate the expression of CRA in animal tissue.
The immunogenicity of enterobacterial common antigen (CA)-treated horse or mouse erythrocytes was determined in Swiss white albino mice by comparing survival rates with control mice, immunized with P. aeruginosa fraction-treated RBC and challenged in parallel with 10 LD50 S. typhimurium. The administration of small amounts of CA on horse, but not mouse, RBC significantly delayed mortality; protection was only marginally less than that evoked with 12-fold larger amounts of CA in the absence of RBC. Survival in infected animals was transient; independent of immunogen or control preparation employed, all mice were dead by day 15 after challenge.
Organs of Swiss white albino and C57BL/6Ha mice were assessed for an antigen (CRA) which cross-reacts with common enterobacterial antigen (CA). To this end, supernatant fluids (HKS) and ethanol-soluble fractions (ES) of heated homogenates of spleens, kidneys, and livers were examined for their capacities to react with CA hemagglutinins and to engender humoral and cellular events in the rabbit. The immunogenicity of CRA in the rabbit can not be predicted on the basis of CA hemagglutinin neutralization studies alone; although CRA was identified in the liver extracts of both mouse strains, according to this parameter, only the liver fraction of Swiss white albino mice elicited significant numbers of rosette-forming cells (RFC) in the spleens of rabbits. Also, kidney fractions, which primed the rabbits for booster with CA, were less effective in stimulating RFC in the spleens failed to inhibit CA hemagglutination and did not prime rabbits for a CA hemagglutinin response, these same preparations clearly evoked RFC in rabbit spleens. Thus, the antigenicity and immunogenicity of CRA in target organs of mice reflect the mouse strain, extraction procedure, and testing method employed.
Organs of gnotobiotic mice were assessed for an Ag (CRA) which cross-reacts with common enterobacterial Ag(CA). To this end, extracts of homogenates of spleens, livers, paired kidneys and colons were examined for their capacities to engender humoral and cellular events in rabbits. The immjnogenicity of CRA in the rabbit cannot be predicted on the basis of CA hemagglutinin-inhibition studies alone. According to this parameter, CRA was present in mouse spleens, livers and paired kidneys but absent in colons. However, the identical preparations, including colons, primed rabbits to engender specific CA hemaglutinins after a single administration of enterobacterial CA. Also, spleens of these same rabbits were colonized with rosette-forming cells against sheep red blood cells treated with various enterobacterial sources of CA. These findings may account, in part, for the apparent refractiveness or equivocal response mice have to administered CA and infectious challenge.