Production of auto-anti-idiotypic antibody during the normal immune response

Bhogal, B.S.; Karkhanis, Yashwant D.; Bell, M K; Sánchez, Pilar Fernández; Zemcik, Barbara A.; Siskind, Gregory W.; Thorbecke, G. J.

doi:10.1016/0008-8749(86)90189-9

Cited by 15 publications

(3 citation statements)

References 22 publications

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“…In the present system collagen-specific suppressor T cells could have suppressed antibody production, particularly of the IgG2 class, or might have prevented the sensitization of T cells directly involved in the initiation and maintenance of arthritis. Alternatively, production of anti-idiotypic autoantibody has been postulated to depress specificially the IgM and IgG immune response after systemic challenge of fed animals with an immunizing dose of antigen (39,40). Although in the present study the effect of type II collagen feeding on the magnitude of the humoral anti-collagen response is not marked, it is still possible that anti-idiotypic regulation could have suppressed a part of the response critical for the induction of CIA by virtue of its specificity.…”

Section: Discussioncontrasting

confidence: 42%

Suppression of type II collagen-induced arthritis by intragastric administration of soluble type II collagen.

Nagler‐Anderson¹,

Bober²,

Robinson³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

312

156

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Although oral administration of protein antigens may lead to specific immunologic unresponsiveness, this method of immunoregulation has not been applied to models of autoimmune disease. Type II collagen-induced arthritis is an animal model of polyarthritis induced in susceptible mice and rats by immunization with type II collagen, a major component of cartilage. Intragastric administration of soluble type II collagen, prior to immunization with type II collagen in adjuvant, suppresses the incidence of collagen-induced arthritis. Administration of denatured type II collagen has no observable effect on the incidence or severity of the disease. The overall magnitude of the antibody response is not significantly reduced in collagen-fed mice as compared to controls. While the isotype distribution of the anti-collagen antibodies is similar in the two groups, there is a tendency toward reduced IgG2 responses in the collagen-fed mice.Type II collagen-induced arthritis (CIA) is an animal model of polyarthritis induced in susceptible mice and rats by immunization with type II collagen (1, 2). Type II collagen is the major matrix protein of hyaline cartilage. The similarity of the histopathologic changes observed in CIA to those seen in human rheumatoid arthritis has centered interest on the contribution of collagen autoimmunity to the pathogenesis of the human disease. Although humoral and cellular immunity to type II collagen have been shown in CIA, the precise contribution of each to the development of disease has not been established. While T cells have been shown to recognize undenatured and denatured type II collagen (3), the humoral response is restricted to the undenatured, nonrepeating helical antigenic determinants of the collagen molecule (3, 4

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Section: Discussioncontrasting

confidence: 42%

Suppression of type II collagen-induced arthritis by intragastric administration of soluble type II collagen.

Nagler‐Anderson¹,

Bober²,

Robinson³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

312

156

View full text Add to dashboard Cite

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“…Isolated reports suggest that tolerance to SRBC and certain contact sensitizing agents can be transferred using serum from antigen-fed mice [214][215][216][217]. Regulation of immunity by anti-idiotypic antibody also has been described in mice tolerized by portal vein inoculation of allogeneic lymphocytes [218].…”

Section: F Other Mechanismsmentioning

confidence: 99%

Oral Tolerance and TGF-β -Producing Cells

Faria¹,

Weiner²

2006

IADT

100

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Multiple mechanisms have been proposed to explain the immune hyporesponsiveness to fed antigens, a phenomenon named oral tolerance. Low doses of orally administered antigen are reported to favor active suppression with the generation of regulatory cells, whereas high doses would favor clonal anergy/deletion. A major conceptual advance in oral tolerance has been the demonstration that TGF-beta plays a central role in oral tolerance as a mediator secreted by Th3 cells. In addition, recent pieces of evidence suggest that TGF-beta may be a primary link between distinct populations of regulatory T cells that are induced by feeding. Conversion of CD4+CD25- into CD4+CD25+ T cells by the expression of FoxP3 involves TGF-beta. A membrane-bound form of TGF-beta (containing latency-associated peptide - LAP) has also been described and LAP+ CD4+ T cells mediate suppression in the gut by a TGF-beta-dependent mechanism. Most of these regulatory T cells are anergic cells indicating that anergy may be also related to Treg induction. Moreover, deletional events taking place in the gut mucosa induce TGF-beta production by either macrophages that phagocyte apoptotic cells or by the dying T cells. Thus, it appears that TGF-beta-producing cells are not only crucial for oral tolerance, but they may be master regulators of most of the mechanisms triggered by antigen feeding.

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“…[5] There are reports that secondary antibodies, just as proposed in the "Jerne network theory" have been detected. [6,7,8,9]…”

Section: Covid-19 Infection or Vaccinationmentioning

confidence: 99%

Jerne's “immune network theory”, of interacting anti‐idiotypic antibodies applied to immune responses during COVID‐19 infection and after COVID‐19 vaccination

Kurbel

2023

BioEssays

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Niels Kaj Jerne has proposed the “immune network theory” of interactions among anti‐idiotypic antibodies, able to interfere with humoral responses to certain antigens. After the occurrence of the primary generation of antibodies, against an antigenic epitope, idiotypes of these antibodies induce anti‐idiotypic antibodies that modulate the intensity of the first response, and so on. Adverse effects following SARS‐COV‐2 COVID‐19 vaccines are occasionally similar to the symptoms of COVID‐19 infection. Rare events linked to SARS‐CoV‐2 vaccines also resemble some rarely reported COVID‐19 complications. Safety data from product information by European Medicines Agency suggest that spectra do overlap for four main vaccines. The proposition is that vaccine events and COVID‐19 complications are related to anti‐idiotypic antibodies whose spatial shape can lead to interactions with ACE2 molecules, in individuals with a prolonged Spike protein synthesis. The vaccines target cells by their affinity to the vaccine vector, or to engulf lipid nanoparticles. Anti‐idiotypic antibodies shaped similarly to the Spike protein possibly interact with ACE2 molecules and cause diverse signs and symptoms.

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Production of auto-anti-idiotypic antibody during the normal immune response

Cited by 15 publications

References 22 publications

Suppression of type II collagen-induced arthritis by intragastric administration of soluble type II collagen.

Suppression of type II collagen-induced arthritis by intragastric administration of soluble type II collagen.

Oral Tolerance and TGF-β -Producing Cells

Jerne's “immune network theory”, of interacting anti‐idiotypic antibodies applied to immune responses during COVID‐19 infection and after COVID‐19 vaccination

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Production of auto-anti-idiotypic antibody during the normal immune response

Cited by 15 publications

References 22 publications

Suppression of type II collagen-induced arthritis by intragastric administration of soluble type II collagen.

Suppression of type II collagen-induced arthritis by intragastric administration of soluble type II collagen.

Oral Tolerance and TGF-&#946; -Producing Cells

Jerne's “immune network theory”, of interacting anti‐idiotypic antibodies applied to immune responses during COVID‐19 infection and after COVID‐19 vaccination

Contact Info

Product

Resources

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Oral Tolerance and TGF-β -Producing Cells