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Epitope-specific recognition of type II collagen by rheumatoid arthritis antibodies is shared with recognition by antibodies that are arthritogenic in collagen-induced arthritis in the mouse.
Arthritis Rheum. 2002 Sep; 46(9):2339-48.AR

Abstract

OBJECTIVE

To analyze the fine specificity of IgG autoantibodies in sera from rheumatoid arthritis (RA) patients for type II collagen (CII) epitopes that are arthritogenic in collagen-induced arthritis (CIA), a relevant murine model of RA.

METHODS

For enzyme-linked immunosorbent assay (ELISA) analysis of conformation-dependent autoantibody binding, recombinant chimeric collagens that harbor the respective CII epitopes as an insertion within the frame of a constant type X collagen triple helix were constructed. In addition, synthetic peptides mimicking the native collagen structures were applied for the first time in the ELISA assessment of humoral CII autoimmunity.

RESULTS

The pathogenicity of IgG responses to certain CII determinants in CIA was demonstrated by arthritis development in BALB/c mice upon the combined transfer of 2 mouse monoclonal antibodies specific for precisely mapped conformational CII epitopes (amino acid residues 359-369 [C1(III)] and 551-564 [J1]), whereas antibodies to another epitope (F4) were not arthritogenic. To test whether human autoimmune responses are similarly directed to these conserved CII determinants, serum IgG was analyzed. The prevalence of sera with increased IgG binding to the C1(III) epitope was significantly higher in RA compared with sera from healthy donors or from patients with other rheumatic conditions, e.g., osteoarthritis (OA), systemic lupus erythematosus (SLE), or relapsing polychondritis (RP), whereas levels of antibodies specific for the nonarthritogenic F4 epitope were associated with OA rather than RA.

CONCLUSION

Autoimmunity to CII, although detectable in different rheumatic conditions, differs in fine specificity between distinct disease entities. In RA, in contrast to degenerative joint disease, RP, and SLE, autoantibody responses are directed to an evolutionary conserved CII structure that is also targeted by pathogenic autoimmune responses in murine models of arthritis.

Authors+Show Affiliations

Burkhardt H
Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Germany. harald.burkhardt@med3.imed.uni-erlangen.de
Koller T
No affiliation info available
Engström A
No affiliation info available
Nandakumar KS
No affiliation info available
Turnay J
No affiliation info available
Kraetsch HG
No affiliation info available
Kalden JR
No affiliation info available
Holmdahl R
No affiliation info available

MeSH

AnimalsAntibodies, MonoclonalAntibody SpecificityArthritisArthritis, RheumatoidAutoantibodiesCollagen Type IICollagen Type IIIEpitopesHumansImmunoglobulin GLupus Erythematosus, SystemicMiceMice, Inbred BALB COsteoarthritisPolychondritis, RelapsingProtein ConformationRecombinant Fusion ProteinsRecombinant Proteins

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12355481

Citation

Burkhardt, Harald, et al. "Epitope-specific Recognition of Type II Collagen By Rheumatoid Arthritis Antibodies Is Shared With Recognition By Antibodies That Are Arthritogenic in Collagen-induced Arthritis in the Mouse." Arthritis and Rheumatism, vol. 46, no. 9, 2002, pp. 2339-48.
Burkhardt H, Koller T, Engström A, et al. Epitope-specific recognition of type II collagen by rheumatoid arthritis antibodies is shared with recognition by antibodies that are arthritogenic in collagen-induced arthritis in the mouse. Arthritis Rheum. 2002;46(9):2339-48.
Burkhardt, H., Koller, T., Engström, A., Nandakumar, K. S., Turnay, J., Kraetsch, H. G., Kalden, J. R., & Holmdahl, R. (2002). Epitope-specific recognition of type II collagen by rheumatoid arthritis antibodies is shared with recognition by antibodies that are arthritogenic in collagen-induced arthritis in the mouse. Arthritis and Rheumatism, 46(9), 2339-48.
Burkhardt H, et al. Epitope-specific Recognition of Type II Collagen By Rheumatoid Arthritis Antibodies Is Shared With Recognition By Antibodies That Are Arthritogenic in Collagen-induced Arthritis in the Mouse. Arthritis Rheum. 2002;46(9):2339-48. PubMed PMID: 12355481.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epitope-specific recognition of type II collagen by rheumatoid arthritis antibodies is shared with recognition by antibodies that are arthritogenic in collagen-induced arthritis in the mouse. AU - Burkhardt,Harald, AU - Koller,Tobias, AU - Engström,Ake, AU - Nandakumar,Kutty Selva, AU - Turnay,Javier, AU - Kraetsch,Hans G, AU - Kalden,Joachim R, AU - Holmdahl,Rikard, PY - 2002/10/2/pubmed PY - 2002/11/26/medline PY - 2002/10/2/entrez SP - 2339 EP - 48 JF - Arthritis and rheumatism JO - Arthritis Rheum VL - 46 IS - 9 N2 - OBJECTIVE: To analyze the fine specificity of IgG autoantibodies in sera from rheumatoid arthritis (RA) patients for type II collagen (CII) epitopes that are arthritogenic in collagen-induced arthritis (CIA), a relevant murine model of RA. METHODS: For enzyme-linked immunosorbent assay (ELISA) analysis of conformation-dependent autoantibody binding, recombinant chimeric collagens that harbor the respective CII epitopes as an insertion within the frame of a constant type X collagen triple helix were constructed. In addition, synthetic peptides mimicking the native collagen structures were applied for the first time in the ELISA assessment of humoral CII autoimmunity. RESULTS: The pathogenicity of IgG responses to certain CII determinants in CIA was demonstrated by arthritis development in BALB/c mice upon the combined transfer of 2 mouse monoclonal antibodies specific for precisely mapped conformational CII epitopes (amino acid residues 359-369 [C1(III)] and 551-564 [J1]), whereas antibodies to another epitope (F4) were not arthritogenic. To test whether human autoimmune responses are similarly directed to these conserved CII determinants, serum IgG was analyzed. The prevalence of sera with increased IgG binding to the C1(III) epitope was significantly higher in RA compared with sera from healthy donors or from patients with other rheumatic conditions, e.g., osteoarthritis (OA), systemic lupus erythematosus (SLE), or relapsing polychondritis (RP), whereas levels of antibodies specific for the nonarthritogenic F4 epitope were associated with OA rather than RA. CONCLUSION: Autoimmunity to CII, although detectable in different rheumatic conditions, differs in fine specificity between distinct disease entities. In RA, in contrast to degenerative joint disease, RP, and SLE, autoantibody responses are directed to an evolutionary conserved CII structure that is also targeted by pathogenic autoimmune responses in murine models of arthritis. SN - 0004-3591 UR - https://www.unboundmedicine.com/medline/citation/12355481/Epitope_specific_recognition_of_type_II_collagen_by_rheumatoid_arthritis_antibodies_is_shared_with_recognition_by_antibodies_that_are_arthritogenic_in_collagen_induced_arthritis_in_the_mouse_ DB - PRIME DP - Unbound Medicine ER -