The enhancement of antibody response by the use of adjuvants in rabbits immunized with purfied plant viruses.
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A method for the production of antibodies specifically directed against penicillin is described. The inability of this antibody to significantly reduce the antibiotic activity of penicillin is noted. Evidence to show the variability of specificities of various sera, some directed for the most part against the side chain, others against the nucleus is presented. Studies on serum fractions separated electrophorectically indicate that the antibody migrates in the fast gamma-globulin and beta-globulin fractions and requires dextran or albumin to effect agglutination. The inability of penicilloic acid, an hydrolysis product of penicillin to provoke antibody formation despite its ability to inhibit the antibody is shown and the implications of this observations are discussed.
High molecular weight (19S) gamma-globulin produces passive cutaneous anaphylaxis (PCA) reactions with its specific antiserum only when it is used as intravenous antigen. Reversed PCA reactions cannot be produced when the 19S protein is injected intradermally in contradistinction to the results with 7S gamma-globulin. Antibodies of the high molecular weight class, when injected intradermally, also failed to give PCA reactions following antigen injection. Heterophile antibodies from the sera of patients with infectious mononucleosis, demonstrated to be entirely of the 19S type, gave negative reactions, while 7S heterophile antibodies from guinea pig did give reactions following intravenous injection of sheep cells. Anti-B isoagglutinins of the 19S class failed to react, while those of the 7S class of similar titer gave clear reactions following the injection of B substance. Evidence was obtained that 19S antibodies were capable of inhibiting the PCA reactions obtained with the 7S type, indicating that interaction with antigen occurred. The failure to elicit PCA reactions appeared to be due to an inability to fix to guinea pig tissues in a manner similar to that known for 7S antibodies and gamma-globulin.
In earlier observations with the picryl system, it was concluded that contact sensitivity was a form of delayed (cellular) hypersensitivity to conjugates of sensitizer with autologous proteins indistinguishable in its immunological mechanism from other classical forms of delayed hypersensitivity to proteins. This conclusion has been confirmed and extended with the picryl and chlorbenzoyl chloride systems. 1. It is shown that to induce a state of contact sensitivity, the minimal necessary amounts of hapten are of the same order of magnitude, whether this hapten is conjugated with protein or the free reactive chemical itself. From this, it is evident that contamination of conjugates with small amounts of unreacted sensitizer plays no part in the induction of contact reactivity by the conjugate. With the dinitrophenyl system, no contact sensitivity could be induced by the conjugates used; possible reasons for this discrepancy are discussed. 2. Animals sensitized to contact by homologous conjugate can be completely desensitized by injections of such a conjugate in large amount; a similar injection schedule has no effect on the contact sensitivity of animals sensitized with the free reactive sensitizer. 3. The capacity of heterologous (ovalbumin) conjugates to evoke anti-hapten antibodies is shown to be greater than that of homologous (guinea pig seralbumin) conjugates: the reverse is true of their capacity to induce delayed reactivity. 4. Evidence is brought forward to suggest that in animals sensitized with homologous albumin conjugates, the specificity of the delayed reaction involves more than the hapten alone, even though the carrier protein is non-antigenic on its own. The contrast with the apparent lesser specificity of the antibodies later produced is discussed.
Experimental elimination of mast cells from the peritoneal tissues of the rat by distilled water treatment inhibited the increase of vascular permeability which normally follows a passively induced antigen-antibody reaction in peritoneal tissue. Thus mast cells may contribute to the initiation of inflammation which follows antigen-antibody reactions.
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