Lack of involvement of auto-anti-idiotypic antibody in the regulation of oscillations and tolerance in the antibody response to levan

Hiernaux, Jean; Chiang, Judy; Baker, Phillip J.; DeLisi, Charles; Prescott, Benjamin

doi:10.1016/0008-8749(82)90225-8

Cited by 13 publications

(5 citation statements)

References 41 publications

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“…The augmentable PFCs, which are responsible for the overshooting, have in most cases been shown to be terminally differentiated B cells which are blocked by auto-anti-idiotypic (auto-antiid) antibodies attached to their surface [9,20,48]. Evidence exists that auto-antiid B cells are under T helper (Th) control [2,21,24,28,49,53], and therefore it dan reasonably be hypothesized that priming hosts with NMB triggers a mechanism that activates Ta cells specific for those B cells which produce anti-id antibodies. These B cells, according to the network theory [27], are internal images of the antigen and bind anti-PC antibodies.…”

Section: Discussionmentioning

confidence: 99%

Immunoresponses to Neisseria meningitidis epitopes: in vivo analysis of immunocompetent cells involved in suppression of secondary response to phosphorylcholine

Faro

Prado

Lareo

et al. 1987

Med Microbiol Immunol

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The immune response to phosphorylcholine (PC) antigens has been extensively studied in recent years. Neisseria meningitidis serogroup B M986 (NMB) was recently reported to induce a PC-specific plaque-forming cell (PFC) immuno-response in mice, a characteristic useful for the study of immunomodulating properties of N. meningitidis. With this technique, priming mice with low doses of NMB has been shown greatly to impair their ability, one month after priming, to mount an anti-PC response induced by NMB; this suppression is permanent, does not involve switching from IgM to another immunoglobulin class, transiently affects the T15 idiotype expression and is carrier specific. We report, based on an analysis of spleen cells from NMB-primed mice in an adoptive transfer model, that this suppression does not appear to be mediated by B lymphocytes nor does it seem to be under the direct control of T lymphocytes; rather, it involves radio-resistant cells. Additionally, our results show that NMB modulates the idiotype composition of the anti-phosphorylcholine response, probably by enhancing the expression of so called hapten-augmentable PFC. These results demonstrate that NMB can interfere effectively with the immune response in a variety of ways.

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Section: Discussionmentioning

confidence: 99%

Immunoresponses to Neisseria meningitidis epitopes: in vivo analysis of immunocompetent cells involved in suppression of secondary response to phosphorylcholine

Faro

Prado

Lareo

et al. 1987

Med Microbiol Immunol

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“…A. Rudbach, Ribi Immunochem Research, Hamilton, Mont. ), bacterial dextran B1355, and SSS-III used as well as the methods by which they were prepared have been described elsewhere (3,8,26,47). Type II Streptococcus pneumoniae R36A ATCC 11733 was obtained from the American Type Culture Collection (Rockville, Md.).…”

Section: Methodsmentioning

confidence: 99%

“…We also examined whether low responsiveness to a variety of amplifier T (TA) cell activity involved in the antibody response to SSS-Ill (2,4,56), or (ii) an alteration in the kinetics for the antibody response and the capacity to develop immunological memory to more complex antigens such as bacterial lipopolysaccharide (LPS) (25,28,30,46,58). Auto-anti-idiotypic antibodies have been detected during the normal immune responses to both polysaccharide antigens (10,14,17,26) and hapten coupled to polysaccharide carriers (51). It has been suggested that CD5 (Ly-1+) B cells play a key role in the production of auto-anti-idiotypic antibody (24,32).…”

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confidence: 99%

Characterization of the immunodeficiency of RIIIS/J mice: immune response to polysaccharide antigens

et al. 1990

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RIIIS/J mice lack an autosomal dominant gene(s) that influences the magnitude of the antibody response to several polysaccharide antigens of bacterial origin. Low responsiveness is demonstrable whether polysaccharide is administered as a T-helper-cell-independent or-dependent antigen conjugated to an immunogenic carrier; however, RIIS/J mice make good anti-hapten antibody responses to haptenated polysaccharides. The low antibody responses of RIIIS/J mice to type III pneumococcal polysaccharide do not appear to be the results of an imbalance in the activity of regulatory T lymphocytes. Compared with other strains of mice, RIIIS/J mice elicit low antibody responses to lipopolysaccharide (LPS). They do not develop a cyclic primary or secondary antibody response to Escherichia coli 0113 LPS; the latter is not due to a lack of mitogenic response to E. coli 0113 LPS. They also produce auto-anti-idiotypic antibody after being immunized with trinitrophenyl-Ficoll.

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“…In our model we also have an oscillating mode O. Oscillatory immune responses are found in various experiments in vivo and in vitro [9][10][11]. Most of these are devoted to study immune response to a non-proleferating antigen, such as LPS (lipopolysaccharide, a sugar molecule) [9,10] or bacterial levan [14]. Cyclic response of T and B cells are found.…”

Section: Comparison To Biological Datamentioning

confidence: 99%

“…A time delay differential equation model of this process was proposed by Grossman et al [12]. Other feedback mechanisms that have been proposed, are the presence of auto-anti-idiotypic antibodies according to Jerne's network hypothesis and the regulatory effects of T helper cells [13,14].…”

Section: Comparison To Biological Datamentioning

confidence: 99%

The transition between immune and disease states in a cellular automaton model of clonal immune response

Bezzi

Celada

Ruffo

et al. 1997

Physica A: Statistical Mechanics and its Applications

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In this paper we extend the Celada-Seiden (CS) model of the humoral immune response to include infectious virus and cytotoxic T lymphocytes (cellular response). The response of the system to virus involves a competition between the ability of the virus to kill the host cells and the host's ability to eliminate the virus. We find two basins of attraction in the dynamics of this system, one is identified with disease and the other with the immune state. There is also an oscillating state that exists on the border of these two stable states.Fluctuations in the population of virus or antibody can end the oscillation and 1 drive the system into one of the stable states. The introduction of mechanisms of cross-regulation between the two responses can bias the system towards one of them. We also study a mean field model, based on coupled maps, to investigate virus-like infections. This simple model reproduces the attractors for average populations observed in the cellular automaton. All the dynamical behavior connected to spatial extension is lost, as is the oscillating feature.Thus the mean field approximation introduced with coupled maps destroys oscillations.

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Lack of involvement of auto-anti-idiotypic antibody in the regulation of oscillations and tolerance in the antibody response to levan

Cited by 13 publications

References 41 publications

Immunoresponses to Neisseria meningitidis epitopes: in vivo analysis of immunocompetent cells involved in suppression of secondary response to phosphorylcholine

Immunoresponses to Neisseria meningitidis epitopes: in vivo analysis of immunocompetent cells involved in suppression of secondary response to phosphorylcholine

Characterization of the immunodeficiency of RIIIS/J mice: immune response to polysaccharide antigens

The transition between immune and disease states in a cellular automaton model of clonal immune response

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