CAPACITY OF MYCOBACTERIAL WAX D AND ITS SUBFRACTIONS TO INDUCE ADJUVANT ARTHRITIS IN RATS

The following points may be deduced from this investigation: (1) The quantity of a chemically defined component of wax D which is present in a given inoculation of adjuvant determines the incidence of adjuvant arthritis. (2) This component is a mycolic acid ester of a peptide-linked polysaccharide which resembles the mucopeptides of mycobacterial cell walls. (3) Only waxes D, or their ultracentrifugal subfractions, in which the peptide complex contains the amino acids: alanine, glutamic and mcso-α, ε-diaminopimelic in a molecular ratio of 3:2:2 arc effective arthritogens. (4) These criteria are the same as those reported by other investigators for the adjuvant effect upon delayed hypersensitivity reactions in guinea pigs, both to innocuous protein antigens and to antigens causing autoimmune diseases such as allergic encephalomyelitis. (5) Dinitrophenylation of wax D does not interfere with either its arthritogenicity or its adjuvant effect. (6) Acetylation of wax D destroys its arthritogenicity and antigenicity, and that of its chromatographically separated subfractions. (7) This is contrary to the reported action of acetylation upon the adjuvant effect in delayed hypersensitivity responses in guinea pigs. Acetylated wax D and the AD subfractions containing amino acids still showed an adjuvant effect. (8) It must be concluded that what is adequate for the adjuvant effect is not always adequate for induction of an immediate hypersensitivity response or for arthritis induction. This difference could be cither quantitative, or qualitative, or both. (9) Acetylated subfractions which contained amino acids protected rats against an arthritogcnic challenge. (10) Evidence is presented favoring the view that antigenic determinants for adjuvant arthritis may be present in either the peptide or the polysaccharide moieties of wax D or both. © 1969 S. Karger AG, Basel.