Abstract
Discussion and Summary
In discussion of autoimmunity there is frequently a suggestion that appropriate injury of tissue can result in the appearance of new antigenic structures recognized as foreign by the host (6, 7). It has been reported also that tissue structures can be rendered immunogenic when complexed with bacterial components (8). The group A streptococcus has been especially implicated. The present studies were designed to detect an antigenic component in rabbit dermal connective tissue, injured with group A streptococcal cell wall fragments, which reflects either a modified tissue structure or a complex of tissue and bacterial antigen.
The results demonstrate that a “new” antigenic structure (line B) is formed in injured connective tissue; however, this component is not unique to group A streptococcal cell wall lesions since it is also found in lesions induced with endotoxin, Freund's adjuvant, or turpentine. This antigen is not detected in serum, PMN, PMN lysosomes, alveolar macrophages, spleen cells, or extracts of normal skin. The further characterization, distribution, and possible function of this component has not been done. We have been unable to detect an autoimmune response against this or any other component of rabbit skin (Jones and Schwab, submitted for publication). The spur line (C to C) observed with antilesion BS fraction and anti-PMN when tested with PMN may also represent a modification (loss) of a PMN antigenic structure in connective tissue lesions.
The experiments described here were made with pooled antisera and pooled antigens, but serum from individual guinea pigs immunized with extracts of individual rabbit tissue gave similar results. The possible confusion of isoantigenic differences between rabbits was controlled by comparing normal and lesion skin tissue taken from opposite flanks of the same animal.
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