Idiotypes, anti-idiotypes, and autoimmunity.

M J Rico; R P Hall

doi:10.1016/s0190-9622(88)70212-1

Home/Archive/PubMed

PubMed · 3049705

Idiotypes, anti-idiotypes, and autoimmunity.

M J Rico·R P Hall

View original source ↗Export metadata ↓

Abstract

Over the past two decades it has become clear that the ability of a host to generate antibodies against a wide variety of potential antigens is due to structural diversity in the antibody molecule within the variable region. This diversity results in sites within the molecule that are themselves immunogenic. These immunogenic sites are called idiotopes, and the collection of idiotopes on a single antibody molecule determines that antibody's idiotype. The idiotype of an antibody molecule is defined serologically by a second antibody termed an anti-idiotype. Anti-idiotypic antibodies can recognize antibody molecules bearing similar or identical structures within the variable regions, which are often on or near sites of antigen binding. Investigation into the nature of idiotype and anti-idiotype interactions has increased our knowledge of antibody structure, antigen-antibody interactions, the regulation of antibody production, and the nature of autoimmune disorders. This review will discuss the nature of idiotypes and anti-idiotypes and their potential role in the diagnosis, management, and treatment of autoimmune, infectious, and malignant diseases.

Explore related subjects

Antibodies, Anti-Idiotypic Antibody Specificity Autoimmune Diseases Cross Reactions Humans Immunoglobulin Idiotypes Molecular Structure Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

M J Rico, R P Hall. 1988. Idiotypes, anti-idiotypes, and autoimmunity.. https://doi.org/10.1016/s0190-9622(88)70212-1

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Application of a combined protocol for rational request and utilization of antibody assays improves clinical diagnostic efficacy in autoimmune rheumatic disease.

CONTEXT: Because of a marked increase in the number of requests for antinuclear antibodies, anti-extractable nuclear antigen antibodies, and anti-double-stranded DNA antibodies for the diagnosis of autoimmune rheumatic disease, guidelines have been proposed for their appropriate use. OBJECTIVE: To evaluate in terms of clinical efficacy and cost-benefit ratio the outcome of applying a protocol for the diagnosis of autoimmune rheumatic disease. DESIGN: A diagnostic protocol for the rational utilization of second-level tests (anti-extractable nuclear antigen antibodies and anti-double-stranded DNA antibodies) was applied at Hospital Polyclinic beginning January 2004. The appropriateness of 685 consecutive requests received at the clinical pathology laboratory from January to June 2004 was assessed. Patients who underwent these laboratory tests were followed up for 12 months after blood sample drawing. RESULTS: Introduction of the protocol led to a significant reduction in the number of second-level tests prescribed (27.9% vs 49.5% for anti-extractable nuclear antigen antibodies; 27.5% vs 56.6% for anti-double-stranded DNA antibodies). After the period of observation, none of the 163 patients who had negative results on the first-level test and were asymptomatic, for whom second-level tests had not therefore been performed, were found to have autoimmune rheumatic disease. In 90.5% (77/85) of patients positive for the second-level tests, clinical confirmation of autoimmune rheumatic disease was obtained. CONCLUSIONS: Not only did application of the diagnostic protocol reduce the number of second-level tests performed but it also increased their specificity. Our data thus indicate that the use of shared guidelines by clinical and laboratory specialists yields satisfactory results.

Antibodies, Anti-Idiotypic↗

PubMed2006

Humoral immune response and immunoglobulin G Fc receptor genotype are associated with better clinical outcome following idiotype vaccination in follicular lymphoma patients regardless of their response to induction chemotherapy.

We have reported that anti-idiotype antibody response and FcgammaRIIIa 158 valine/valine (V/V) genotype both correlate with better outcome in a group of 136 follicular lymphoma patients receiving idiotype vaccination after induction chemotherapy. Here, we examined whether this correlation is related in any way to the chemotherapy response. In patients with complete response (CR), the 5-year progression-free survival (PFS) was 69% for patients with antibody response and/or V/V genotype, while the PFS was only 40% for patients with neither; the median time to progression (TTP) was 10.47 versus 3.46 years (P=.012). In patients with partial response (PR), the 5-year PFS was 57% for patients with antibody response and/or V/V genotype, and 17% for patients with neither; the median TTP was not reached versus 1.31 years (P=.001). This study further confirms the strong association of clinical outcome with antibody response and with the functionally more active form of the Fc receptor in patients receiving idiotype vaccination regardless of their response to induction chemotherapy.

Antibodies, Anti-Idiotypic↗

PubMed2006

Human beta-defensin-3 induction in H. pylori-infected gastric mucosal tissues.

AIM: To examine human beta-defensin-3 (hBD-3) expression in inflamed gastric mucosal tissues or MKN45 gastric cancer cells with or without H. pylori infection for better understanding the innate immune response to H. pylori. METHODS: We used reverse transcription-polymerase chain reactions and immunohistochemistry to examine hBD-3 expression in inflamed gastric mucosal tissues or MKN45 gastric cancer cells with or without H. pylori. Effects of hBD-3 against H. pylori were also evaluated. RESULTS: The mean mRNA expression of hBD-3 in H. pylori-positive specimens was significantly higher than that in H pylori-negative specimens (P = 0.0002, Mann-Whitney). In addition, unlike uninfected samples, 8 of 15 (53.33%) infected mucosal samples expressed hBD-3 protein. H. pylori dose-dependently induced mRNA expression of hBD-3 in MKN45 cells, an effect inhibited by adding anti-toll-like receptor (TLR)-4 antibody. HBD-3 protein completely inhibited H. pylori growth. CONCLUSION: Our results suggest that like hBD-2, hBD-3 may be involved in the pathophysiology of H. pylori-induced gastritis.

Antibodies, Anti-Idiotypic↗