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PubMed1976

Receptor-blocking factor present in immune serum resembling auto-anti-idiotype antibody.

Previous studies have shown that rabbit antibody-forming cells in the primary and secondary response possess cell-associated antigen-binding receptors. In the present study, we demonstrate that a factor appears in the serum of rabbits following immunization which inhibits the antigen binding of up to 60% of the receptor-bearing antibody-forming cells in both the primary and secondary response. These observations were made on lymph node cells from rabbits primed with either sheep red blood cells (SRBC)3 or 3-nitro-4-hydroxy-5-iodophenylacetic acid coupled to keyhole limpet hemocyanin (NIP-KLH). The inhibitory activity is not associated with anti-SRBC or anti-NIP antibody. In the primary response to SRBC, the antigen binding by day 6 antibody-forming cells is inhibited by the autologous days 7 to 10 inactivated and absorbed serum. In the secondary response to SRBC, the inhibitory factor peaks in the serum around day 10. Later, in both the primary and secondary immune response to SRBC, the inhibitory activity of the serum decreases rapidly. In the primary response to NIP-KLH, the inhibitory activity of the immune sera increased from day 7 through day 14. The receptor-inhibiting factor is antigen specific since the serum from SRBC-primed rabbits inhibits SRBC binding by anti-SRBC antibody-forming cells, but it does not inhibit NIP binding by anti-NIP antibody-forming cells. Similarly, serum from NIP-KLH-primed rabbits inhibits NIP binding by anti-NIP antibody-forming cells, but does not inhibit the SRBC receptor on the anti-SRBC antibody-forming cells. The inhibition is not due to the presence of antihapten or anti-SRBC antibody competing with receptor sites, since the immune sera from one SRBC-primed animal inhibit antigen binding of its own antibody-forming cells, but do not inhibit the antigen binding of antibody-forming cells from other SRBC-primed rabbits.

Animals↗

PubMed1976

Rosette plaques with lymphoid cells from heterozygous rabbits. Ani-hapten antibody-forming cells displaying either one or both b locus surface allelic markers.

A rosette-plaque model was employed to test for the expression of b locus allelic markers at the surface of lymph node lymphocytes (LNL) from heterozygous (b4,6) rabbits, 5 days after immunization with NIP-diphtheria toxoid. Before immunization, in all animals examined, LNL displaying both b4 and b6 determinants at the surface (range 5-20 per cent) were detected, the remainder consisting of cells exhibiting only one or the other determinant. After immunization, five of the thirteen heterozygotes apparently had gone into allelic exclusion as LNL from these animals showed only b4 or b6 rosettes which secreted anti-NIP antibody in the plaque. The eight remaining rabbits remained in allelic inclusion. Since cytophilic uptake of allotype might have contributed to double expression, LNL from immunized animals were treated with pronase to remove surface immunoglobulin. When the stripped cells were cultured overnight in serum-free medium, reappearance of b4, b6, and b4 plus b6 expressing cells was seen. When pronase-stripped cells were incubated in cycloheximide (20 mug/ml) for 5 hr, no allotype synthesis was found but inhibition was relieved when the cells were washed free of the antibiotic. Regrowth resulted in rosette levels similar to those found originally in the three allotype-bearing populations. Stripping the cell surface allotype with pronase, and allowing regrowth of allotype overnight also resulted in one of four animals regaining the ability to express both allotypes at the surface in the plaque-forming situation. Lymphocytes from homozygous controls (b4,4 and b6,6) displayed their own individual allelic markers either when the cells from each were tested alone or in combination, unimmunized or immunized. An additional finding was the apparent lack of allelic preference for NIP in the heterozygotes as approximately similar numbers of cells were found bearing the b4 and b6 marker at the surface in the NIP plaque.

Alleles↗

PubMed1976

Immunological memory after priming with a thymus independent antigen, NIP-ficoll. 4-hydroxy-5-iodo-3-nitrophenylacetyl coupled to polymer of sucrose and epichlorhydrin.

The capacity of mouse spleen fragments to mount an anti-NIP (4-hydroxy-5-iodo-3-nitrophenylacetyl) response in vitro was studied. The fragments came from unprimed, NIP-Ficoll (polymer of sucrose and epichlorhydrin) or NIP-CG (chicken globulin) primed mice. Unprimed spleen fragments from C57BL/6 mice gave a good anti-NIP response to NIP-Ficoll, whereas CBA fragments did not. Priming with NIP-Ficoll made CBA fragments responsive and enhanced slightly the response of C57BL/6 fragments when stimulated with the same antigen. This memory effect could be seen only after a small priming dose. Priming the mice with NIP-Ficoll made their spleen fragments responsive to a protein conjugate of NIP (NIP-CG), but this effect was seen only after priming with a high dose. The antibody class distribution and the kinetics of the appearance of different immunoglobulin classes were similar in the primary and secondary responses in vitro. The peak responses of IgM, IgA and IgG were reached on day eight and the relative amount of IgG was the same in the primary and in the secondary responses. Spleen fragments derived from NIP-CG primed mice produced more IgG anti-NIP antibodies than fragments derived from untreated mice when immunized in vitro with NIP-Ficoll. The amount of IgG was, however, much higher when these fragments were challenged with the homologous antigen, NIP-CG.

Animals↗