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An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Enrichment of malondialdehyde-acetaldehyde antibody in the rheumatoid arthritis joint
Ted R Mikuls1,2, Michael J Duryee1,2, Rafid Rahman2
1Veteran Affairs Nebraska-Western Iowa Health Care System.
Objective:
To characterize the expression of malondialdehdye-acetaldehyde (MAA) adducts and anti-MAA antibody in articular tissues and serum of patients with RA.
Methods:
Paired sera and SF were examined from 29 RA and 13 OA patients. Anti-MAA antibody, RF, ACPA and total immunoglobulin were quantified. SF-serum measures were compared within and between disease groups. The presence and co-localization of MAA, citrulline and select leukocyte antigens in RA and OA synovial tissues were examined using immunohistochemistry.
Results:
Circulating and SF anti-MAA antibody concentrations were higher in RA vs OA by 1.5- to 5-fold. IgG (P < 0.001), IgM (P = 0.006) and IgA (P = 0.036) anti-MAA antibodies were higher in paired RA SF than serum, differences not observed for total immunoglobulin, RF or ACPA. In RA synovial tissues, co-localization of MAA with citrulline and CD19+ or CD27+ B cells was demonstrated and was much higher in magnitude than MAA or citrulline co-localization with T cells, monocytes, macrophages or dendritic cells (P < 0.01).
Conclusion:
Anti-MAA antibodies are present in higher concentrations in the RA joint compared with sera, a finding not observed for other disease-related autoantibodies. Co-localization of MAA and citrulline with mature B cells, coupled with the local enrichment of anti-MAA immune responses, implicates MAA-adduct formation in local autoantibody production.
Insights
Malondialdehyde-acetaldehyde (MAA) adducts and anti-MAA antibodies are elevated in rheumatoid arthritis (RA) joints. These findings suggest MAA adducts contribute to local autoantibody production in RA.
Area of Science:
- Rheumatology
- Immunology
- Biochemistry
Background:
- Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation.
- The role of specific adducts, such as malondialdehyde-acetaldehyde (MAA), and their corresponding antibodies in RA pathogenesis remains to be fully elucidated.
Purpose of the Study:
- To investigate the expression of MAA adducts and anti-MAA antibodies in the synovial tissues and serum of patients with RA.
- To compare these markers between RA and osteoarthritis (OA) patients.
Main Methods:
- Analysis of paired serum and synovial fluid (SF) samples from RA and OA patients.
- Quantification of anti-MAA antibodies, rheumatoid factor (RF), anti-citrullinated protein antibodies (ACPA), and total immunoglobulin.
- Immunohistochemical examination of synovial tissues for MAA adducts, citrulline, and leukocyte markers.
Main Results:
- Anti-MAA antibody concentrations were significantly higher in RA serum and SF compared to OA.
- IgG, IgM, and IgA anti-MAA antibodies were enriched in RA SF relative to serum.
- MAA adducts co-localized with citrulline and B cells (CD19+, CD27+) in RA synovial tissues, more so than with T cells or monocytes.
Conclusions:
- Anti-MAA antibodies show local enrichment within the RA joint, unlike other autoantibodies.
- The co-localization of MAA adducts and citrulline with B cells suggests MAA adducts play a role in local autoantibody production in RA.
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