Changes in affinity of 19 and 7S antibodies at the cellular level in responses to hapten conjugates of varying T dependency

Goidl, Edmond A.; Romano, Thomas J.; Siskind, Gregory W.; Thorbecke, G. J.

doi:10.1016/0008-8749(78)90145-4

Cited by 19 publications

(7 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is worth noting that, in contrast to the results with TNP-BGG, the concentrations of hapten required for optimal augmentation of PFC in the primary and secondary responses to TNP-F were essentially the same. This is consistent with the above interpretation, in that typically antibody responses to TI antigens show a less marked change in affinity with time after immunization or following boosting than do responses to TD antigens [21].…”

Section: Discussionsupporting

confidence: 89%

Production of auto‐anti‐idiotypic antibody during the normal immune response. IV. Studies of the primary and secondary responses to thymus‐dependent and‐independent antigens

Ea¹,

Af²,

Gh³

et al. 1980

Eur J Immunol

Self Cite

View full text Add to dashboard Cite

We have previously shown that hapten-augmentable plaque-forming cells are cells whose secretion of antibody is inhibited by the binding of auto-anti-idiotype antibody to cell surface antigen receptors. Using hapten augmentation of plaque formation, it was shown in the present report that auto-anti-idiotype antibodies are produced during the primary and secondary responses to both thymus-dependent und thymus-independent antigens. In the secondary response to the T-independent antigen trinitrophenylated Ficoll, the rate of appearance of auto-anti-idiotype antibody was faster, and the number of hapten-augmentable plaques was greater than in the primary response suggesting an anamnestic auto-anti-idiotype response. With the T-dependent antigen, trinitrophenylated bovine gamma-globulin, the kinetics and magnitude of the auto-anti-idiotypic antibody response were relatively similar in the primary and secondary responses. However, a lower concentration of hapten was required to reveal the hapten-augmentable plaques in the secondary response. This is in keeping with the usual finding that secondary antibody to T-dependent antigens is of very high affinity. Both direct and indirect hapten-augmentable plaque-forming cells were detected suggesting that the secretion of both IgM and IgG antibodies is regulated by auto-anti-idiotype antibodies. The data are consistent with a role for auto-anti-idiotype antibody in the normal down-regulation of the immune response as suggested by Jerne's network hypothesis.

show abstract

Section: Discussionsupporting

confidence: 89%

Production of auto‐anti‐idiotypic antibody during the normal immune response. IV. Studies of the primary and secondary responses to thymus‐dependent and‐independent antigens

Ea¹,

Af²,

Gh³

et al. 1980

Eur J Immunol

Self Cite

View full text Add to dashboard Cite

show abstract

“…We have previously reported that nude mice immunized with TNP-pneumococcal polysaccharide produced a secondary direct PFC response of greater heterogeneity and higher affinity than that of +/+ littermates (6). When euthymic mice were immunized with T-independent antigens no increase in antibody affinity with time after initial antigen injection was observed (6 and this paper).…”

Section: Discussionmentioning

confidence: 59%

“…The response to TNP-polysaccharide conjugates is thymus independent (3,4) and, in fact, is frequently higher and more heterogeneous with respect to affinity in athymic, as compared with normal, mice (4)(5)(6). It has been suggested that this is a result of the absence of T suppressor cells in athymic mice (5,6). The results in this paper will show that the anti-idiotypic-antibody response, and its resulting regulation of the anti-TNP response, are absent in athymic mice.…”

mentioning

confidence: 99%

Production of auto-anti-idiotypic antibody during the normal immune response to TNP-ficoll. III. Absence in nu/nu mice: evidence for T-cell dependence of the anti-idiotypic-antibody response.

Schrater¹,

Goidl²,

Thorbecke³

et al. 1979

The Journal of Experimental Medicine

View full text Add to dashboard Cite

In previous papers (1, 2) in this series we have presented evidence that an autoanti-idiotypic-antibody response occurs during the normal immune response to a Tindependent antigen. The evidence also suggested that this auto-anti-idiotypic response is involved in the regulation of the immune response. It was established that hapten-augmentable plaque-forming cells (PFC),I defined as antibody-producing cells which could not be detected as PFC in the Jerne assay unless hapten was present during the assay, represented cells whose secretion of antibody was inhibited by bound auto-anti-idiotypic antibody. Furthermore, it was shown that anti-idiotypic antibody can be assayed by its ability to cause hapten-reversible inhibition of plaque formation.In these earlier studies (1, 2) we noted that the magnitude of the response to trinitrophenyl-lys-Ficoll (TNP-F) falls precipitously between days 4 and 7 after immunization in both AKR/J and BALB/c mice (1, 2) and that serum from AKR/ J mice taken 7 d after injection of TNP-F contained anti-idiotypic antibody to antitrinitrophenyl (TNP). An important role for anti-idiotypic antibody in the down regulation of the anti-TNP response was suggested by the presence of haptenaugmentable PFC in spleens taken more than 4 d after immunization. The percentage of hapten-augmentable (anti-idiotype-blocked) PFC arising spontaneously during the immune response to TNP-F in AKR/J mice was 5% on day 4 and 25% on day 5. Moreover, normal AKR/J recipients of syngeneic TNP-F-immune spleen cells plus antigen had a far higher incidence of hapten-augmentable PFC 3 and 4 d after cell transfer (298 and 122%, respectively). The PFC response by such recipients, as detected in the absence of hapten, was lower than that of recipients of normal cells; however, the results of the assay in the presence of hapten showed this apparent decrease to be a result of the blocking of large numbers of PFC by anti-idiotypic

show abstract

“…TNP-conjugated sheep erythrocytes were prepared as described by Rittenberg et al [12]. Indirect PFC were developed with rabbit anti-Ig, while direct PFC development was inhibited by incorporation of goat anti-p [13] into the agar.…”

Section: Enumeration Of Igd-and Ig-bearing Cellsmentioning

confidence: 99%

Physiology of IgD. II. Lack of humoral immune responsiveness in lymph nodes of mice treated with anti‐IgD from birth

Baine

Chen

et al. 1982

Eur J Immunol

Self Cite

View full text Add to dashboard Cite

Previous studies have shown that anti-IgD-suppressed mice give normal primary and secondary splenic plaque-forming cell responses following i.v. challenge, although mice suppressed by the injection of anti-IgD from birth lack IgD-bearing cells in all lymphoid tissue examined. The present studies show that, in contrast, secondary immune responses in regional lymph nodes of such mice, even after i.v. priming with trinitrophenylated B. abortus, respond to a challenge injection in the footpad up to only less than 10% of control levels. When compared with respect to B cell numbers transferred, primed spleen cells from control and anti-IgD-suppressed mice are about equally effective in producing adoptive secondary plaque-forming cell responses in the spleens of recipient mice. Lymph nodes in recipients of anti-IgD-suppressed primed spleen cells show much lower responses than do lymph nodes in recipients of control primed cells, both upon immediate and delayed challenge with antigen in the footpads. It is concluded that the immunodeficiency caused by suppression with anti-IgD is much more marked in peripheral lymph nodes than in the spleen. The possible relationship of these results to the migratory properties of IgD+ as compared to IgD-B cells is discussed.

show abstract

Changes in affinity of 19 and 7S antibodies at the cellular level in responses to hapten conjugates of varying T dependency

Cited by 19 publications

References 34 publications

Production of auto‐anti‐idiotypic antibody during the normal immune response. IV. Studies of the primary and secondary responses to thymus‐dependent and‐independent antigens

Production of auto‐anti‐idiotypic antibody during the normal immune response. IV. Studies of the primary and secondary responses to thymus‐dependent and‐independent antigens

Production of auto-anti-idiotypic antibody during the normal immune response to TNP-ficoll. III. Absence in nu/nu mice: evidence for T-cell dependence of the anti-idiotypic-antibody response.

Physiology of IgD. II. Lack of humoral immune responsiveness in lymph nodes of mice treated with anti‐IgD from birth

Contact Info

Product

Resources

About