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Abatacept treatment reduced granzyme B (GZMB) serum levels in rheumatoid arthritis (RA) patients who responded to therapy. This suggests a potential mechanism for abatacept in preventing joint erosions, though CD28neg T-cells may not be the primary source of GZMB.

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Area of Science:

  • Immunology
  • Rheumatology
  • Molecular Biology

Background:

  • Rheumatoid arthritis (RA) pathogenesis involves joint erosions.
  • Granzyme B (GZMB) is implicated in RA joint erosion.
  • CD28-negative T-cells are a potential source of GZMB.

Purpose of the Study:

  • To evaluate the effect of abatacept therapy on serum GZMB levels in RA patients.
  • To investigate the relationship between GZMB levels, disease activity, and T-cell populations in RA.
  • To explore potential mechanisms of action for abatacept in RA treatment.

Main Methods:

  • Serum GZMB levels were measured using enzyme immunoassay in 53 RA patients before (T0) and 25 patients after 6 months (T6) of abatacept therapy.
  • Disease activity was assessed using DAS28-CRP.
  • Percentages of circulating CD4+CD28neg and CD8+CD28neg T-cells were analyzed.

Main Results:

  • Serum GZMB levels at T0 correlated with DAS28-CRP and CD28neg T-cell percentages.
  • GZMB levels significantly decreased in patients with moderate to good EULAR response to abatacept (p=0.023).
  • No significant change in GZMB levels was observed in non-responders.

Conclusions:

  • Abatacept therapy can decrease serum GZMB levels in responding RA patients.
  • This reduction may contribute to abatacept's ability to prevent radiographic erosions in RA.
  • The lack of correlation with CD28neg T-cells suggests alternative sources for serum GZMB.