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

Ea, Goidl; Af, Schrater; Gh, Thorbecke; Siskind, GW

doi:10.1002/eji.1830101103

Cited by 28 publications

(2 citation statements)

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“…Antigens, Antisera, and Immunization. The preparation of TNP-F and TNP-bovine gamma globulin (BGG) has been described previously (13,15). Animals were immunized by the intravenous injection of 10 #g of TNP-F in saline, or by the intraperitoneal injection of 500/~g…”

Section: Methodsmentioning

confidence: 99%

“…Male C57BL/6 mice, of various ages, were obtained from a colony maintained by the National Institute of Aging at the Charles River Breeding Laboratories, Wilmington, MA.Antigens, Antisera, and Immunization. The preparation of TNP-F and TNP-bovine gamma globulin (BGG) has been described previously (13,15). Animals were immunized by the intravenous injection of 10 #g of TNP-F in saline, or by the intraperitoneal injection of 500/~g…”

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confidence: 99%

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Production of auto-antiidiotypic antibody during the normal immune response. VII. Analysis of the cellular basis for the increased auto-antiidiotype antibody production by aged mice.

Goidl¹,

Choy²,

Gibbons³

et al. 1983

The Journal of Experimental Medicine

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We have previously shown that old mice produce more hapten-augmentable plaque-forming cells (PFC) than do young animals, suggesting a greater auto-antiidiotype antibody (auto anti-Id) component in their immune response. In the present studies this is confirmed serologically. The marked auto-anti-Id response of aged mice can be transferred to lethally irradiated young recipients with spleen but not bone marrow cells from old donors, suggesting that it is an intrinsic property of their peripheral B cell population and that the distribution of Id arising from the bone marrow of old and young mice is similar. In contrast with young mice the auto-anti-Id response of old animals is relatively T cell-independent and old donors do not show an increase in their ability to transfer an auto-anti-Id response after priming with TNP-F. These observations suggest that old mice behave as if already primed for auto-anti-Id production. Irradiated mice reconstituted with bone marrow cells from either young or old donors together with splenic T cells from old donors generate a relatively large auto-anti-Id response, whereas mice reconstituted with bone marrow from either young or old donors together with splenic T cells from young donors produce few hapten-augmentable PFC. It is suggested that differences in Id expression and auto-anti-Id production are the consequences of the interaction of Id (and anti-Id) arising from the marrow with anti-Id (and Id) present in the peripheral T cell population which serves as a repository of information about shifts in Id distribution, resulting from lifelong interactions with environmental and self-antigens.

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Production of auto-antiidiotypic antibody during the normal immune response. VII. Analysis of the cellular basis for the increased auto-antiidiotype antibody production by aged mice.

Goidl¹,

Choy²,

Gibbons³

et al. 1983

The Journal of Experimental Medicine

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Lack of age‐associated auto‐anti‐idiotypic antibody regulation in mucosal‐associated lymph nodes

Szewczuk

Campbell

1981

Eur J Immunol

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It has previously been shown that the loss of immune competence in the splenic B cell population with age may be due to auto‐anti‐idiotypic antibody regulation (M. R. Szewczuk and R. J. Campbell, Nature 1980. 286: 164). In the present study we have investigated the appearance of auto‐anti‐idiotypic antibody on immune B cells from the mucosal‐associated lymph nodes of old and young mice of the same strain. Various aged C57BL/6J male mice were immunized with 500 μg trinitrophenylated bovine gamma globulin (TNP‐BGG) in complete Freund's adjuvant (CFA) intraperitoneally. IgM, IgG and IgA anti‐TNP plaque‐forming cell (PFC) responses in the spleen, mediastinal and mesenteric lymph nodes were assayed for anti‐idiotype‐blocked, hapten‐augmentable PFC, 14 days later. It was found that 8 months or older C57BL/6J male mice produced a significantly high percentage of hapten‐augmentable IgM, IgG and IgA anti‐TNP PFC in the spleen. In contrast, there was a lack of hapten‐augmentable anti‐TNP PFC in the mesenteric and mediastinal lymph nodes with increasing age of the animal. Mice receiving antigen in the footpads and base of the tail also produced a significantly high percentage of hapten‐augmentable IgG PFC in the draining peripheral lymph nodes. TNP‐ε‐amino‐n‐caproic acid (EACA) as hapten was shown to specifically augment anti‐TNP PFC. Immune sera from 15‐month‐old mice caused a specific inhibition of anti‐TNP PFC in vitro. The inhibition of plaque formation was completely reversible by addition of TNP‐EACA as hapten. This PFC inhibitory activity in immune sera lacked anti‐TNP antibody activity, but reacted with anti‐TNP antibody of C57BL/6J origin. Immune sera from 8 month or older mice also revealed anti‐(anti‐TNP F(ab')2 IgG) titer as assayed by passive hemagglutination. Thus, the results of this study indicate a division of the immune system into regulatory compartments. Auto‐anti‐idiotypic antibody may be involved in a down‐regulation of systemic responses but with no apparent effect in the mucosal‐associated lymph nodes.

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Assessment of a functional role of auto‐anti‐idiotypes in idiotype dominance

et al. 1995

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We have used a well-defined idiotypic system, the cross-reactive idiotype of A strain (CRIA) (Ab1) idiotype generated in A/J mice injected with arsonate coupled to keyhole limpet hemocyanin (ARS-KLH), to determine the frequency of precursors for auto-anti-idiotypic antibodies (auto-Ab2) in naive and immunized A/J mice by limiting dilution analysis after polyclonal activation by lipopolysaccharide. In naive animals, the precursor frequencies of auto-Ab2 B cells were below the limit of sensitivity of the technique in the majority of A/J mice, and could be detected in only 20% of the animals. Upon immunization with ARS-KLH, a large increase in auto-Ab2 precursor frequency was observed. This shift in frequency was not found when A/J mice were injected with KLH alone, or when BALB/c mice, which do not express the CRIA idiotype, were injected with ARS-KLH. To study the functional role of the auto-Ab2 B cells, we injected neonatal A/J mice with polyclonal rabbit Ab3 antibodies directed against a recurrent idiotype of auto-Ab2. Thereafter, these mice were injected with ARS-KLH. Although the anti-arsonate response level was normal, the CRIA Ab1 expression was reduced tenfold. Thus, the suppression of auto-Ab2 affects Ab1 dominance. We further show that the presence of maternal Ab1 can strongly modify the immune response of the offspring by inducing higher levels of the idiotype after immunization. Furthermore, IgM anti-arsonate antibodies were detected before immunization with antigen. From these data, we conclude that the affinity of antigen alone cannot explain the dominance of CRIA. Network selection is important in the shaping of the available repertoire.

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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

Cited by 28 publications

References 18 publications

Production of auto-antiidiotypic antibody during the normal immune response. VII. Analysis of the cellular basis for the increased auto-antiidiotype antibody production by aged mice.

Production of auto-antiidiotypic antibody during the normal immune response. VII. Analysis of the cellular basis for the increased auto-antiidiotype antibody production by aged mice.

Lack of age‐associated auto‐anti‐idiotypic antibody regulation in mucosal‐associated lymph nodes

Assessment of a functional role of auto‐anti‐idiotypes in idiotype dominance

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