Next Article in Journal
Biochemical and MALDI-TOF Mass Spectrometric Characterization of a Novel Native and Recombinant Cystine Knot Miniprotein from Solanum tuberosum subsp. andigenum cv. Churqueña
Next Article in Special Issue
Structural Biology of the TNFα Antagonists Used in the Treatment of Rheumatoid Arthritis
Previous Article in Journal
The New Structure of Core Oligosaccharide Presented by Proteus penneri 40A and 41 Lipopolysaccharides
Previous Article in Special Issue
Therapeutics in Osteoarthritis Based on an Understanding of Its Molecular Pathogenesis
Article Menu
Issue 3 (March) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2018, 19(3), 677;

Targeting IgG in Arthritis: Disease Pathways and Therapeutic Avenues

School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510000, China
Department of Medical Biochemistry and Biophysics, Karolinska Institute, 17177 Stockholm, Sweden
Received: 31 December 2017 / Revised: 25 January 2018 / Accepted: 22 February 2018 / Published: 28 February 2018
(This article belongs to the Special Issue Research of Pathogenesis and Novel Therapeutics in Arthritis)
Full-Text   |   PDF [1846 KB, uploaded 28 February 2018]   |  


Rheumatoid arthritis (RA) is a polygenic and multifactorial syndrome. Many complex immunological and genetic interactions are involved in the final outcome of the clinical disease. Autoantibodies (rheumatoid factors, anti-citrullinated peptide/protein antibodies) are present in RA patients’ sera for a long time before the onset of clinical disease. Prior to arthritis onset, in the autoantibody response, epitope spreading, avidity maturation, and changes towards a pro-inflammatory Fc glycosylation phenotype occurs. Genetic association of epitope specific autoantibody responses and the induction of inflammation dependent and independent changes in the cartilage by pathogenic autoantibodies emphasize the crucial contribution of antibody-initiated inflammation in RA development. Targeting IgG by glyco-engineering, bacterial enzymes to specifically cleave IgG/alter N-linked Fc-glycans at Asn 297 or blocking the downstream effector pathways offers new avenues to develop novel therapeutics for arthritis treatment. View Full-Text
Keywords: rheumatoid arthritis; antibodies; collagen; glycosylation; disease pathways; therapy; experimental arthritis rheumatoid arthritis; antibodies; collagen; glycosylation; disease pathways; therapy; experimental arthritis

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Nandakumar, K.S. Targeting IgG in Arthritis: Disease Pathways and Therapeutic Avenues. Int. J. Mol. Sci. 2018, 19, 677.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top