Elicit: Cytokine Response to Abatacept in RA

Cytokine Response to Abatacept in RA

Which cytokines (e.g., TNF-α, IL-2, IFN-γ) change most with abatacept treatment in RA?

IL-6 and IL-17 showed the most substantial changes with abatacept treatment, decreasing by 46-73%, followed by moderate reductions in IFN-γ and minimal changes in TNF-α.

Abstract

Ten studies evaluated cytokine changes following abatacept treatment in RA patients, employing before-after or cohort designs with treatment durations ranging from 16 weeks to over 5 years. Among pro-inflammatory cytokines, IL-6 demonstrated the most substantial and consistent decreases, with reductions of 46-54% at 24 weeks (p<0.001). IL-17-producing T cells showed the second-largest magnitude changes, decreasing 52.6-73% in clinical responders at 6-12 months (p≤0.017), with levels normalizing to those of healthy controls. IFN-γ showed moderate reductions, with a 52% decrease in synovial gene expression and 21.4% decrease in cellular production. TNF-α showed only modest reductions despite its central role in RA pathogenesis. Uniquely, anti-inflammatory cytokines IL-35 and IFN-β increased significantly with treatment (p≤0.0013). Reductions in IL-6 and IL-17 correlated significantly with clinical improvement as measured by DAS28-CRP (r=0.477-0.5, p<0.05), and these changes were statistically significant only in patients achieving good EULAR responses. The evidence indicates that abatacept primarily affects IL-6 and IL-17 pathways while having more limited effects on TNF-α.

Methods

We analyzed 10 sources from an initial pool of 200, using 8 screening criteria. Each paper was reviewed for 7 key aspects that mattered most to the research question.

Records from Elicit search

Data extraction

We asked a large language model to extract each data column below from each paper:

Results

Characteristics of included studies

Study Full text retrieved? Study Type Sample Size Treatment Duration Control Groups Setting
M. Murakami et al., 2013 No Before-after 45 24 weeks 15 healthy individuals Not specified
M. Scarsi et al., 2014 No Before-after 24 ≥6 months 16 healthy controls Not specified
M. Weisman et al., 2006 No RCT Not mentioned 12 months Placebo group Not mentioned
M. Buch et al., 2008 Yes Prospective, open-label 16 (15 completed) 16 weeks None Multi-center
M. Scarsi et al., 2013 No Before-after 24 ≥6 months 16 healthy donors Not specified
M. Alenazy et al., 2021 Yes Before-after 31 ≥6 months 31 RA patients on other treatments, 30 healthy controls Single-center
L. Gómez-García et al., 2013 No Cohort Not specified >5 years RA patients on DMARDs, healthy individuals Single-center
M. Borisova et al., 2017 No Before-after 44 24 weeks 16 healthy individuals Not mentioned
M. Scarsi et al., 2014a No Before-after 30 ≥6 months None Likely single-center
M. Scarsi et al., 2013a No Cohort 42 ≥6 months Not mentioned Likely single-center

Patient populations were relatively homogeneous across studies. Where reported, patients were predominantly female with mean ages ranging from 46.9 to 55 years. Disease duration varied from a median of 2 years to 10 years. Baseline disease activity was generally high, with DAS28 scores ranging from 5.2 to 7.1 where reported. Most patients had failed prior DMARD or biologic therapy. Seropositivity rates were high, with 75-84.4% being RF-positive and/or ACPA-positive.

Clinical response rates were favorable across studies. Good or moderate EULAR responses were achieved in 60-86% of patients, with 52-71% achieving clinical remission or good response.

Cytokines measured across studies

Cytokine levels were assessed using varied methodologies, including ELISA and flow cytometry.

Cytokine Studies Measuring Classification Measurement Type
IL-6 M. Murakami et al., 2013; M. Weisman et al., 2006; M. Buch et al., 2008; L. Gómez-García et al., 2013; M. Borisova et al., 2017 Pro-inflammatory Plasma/serum; gene expression
IL-17 M. Murakami et al., 2013; M. Scarsi et al., 2014; M. Scarsi et al., 2013; M. Alenazy et al., 2021; L. Gómez-García et al., 2013; M. Borisova et al., 2017; M. Scarsi et al., 2014a; M. Scarsi et al., 2013a Th17 Plasma/serum; cellular production
IFN-γ M. Murakami et al., 2013; M. Scarsi et al., 2014; M. Buch et al., 2008; M. Scarsi et al., 2013; L. Gómez-García et al., 2013; M. Scarsi et al., 2013a Th1 Plasma/serum; cellular production; gene expression
TNF-α M. Murakami et al., 2013; M. Weisman et al., 2006; M. Buch et al., 2008; L. Gómez-García et al., 2013; M. Borisova et al., 2017 Pro-inflammatory Serum; gene expression
IL-2 M. Murakami et al., 2013 Th1 Plasma
IL-4 M. Murakami et al., 2013 Th2 Plasma
IL-10 M. Murakami et al., 2013; M. Alenazy et al., 2021 Th2; anti-inflammatory Plasma/serum
Soluble IL-2 receptor M. Weisman et al., 2006 Not specified Serum
IL-1β M. Buch et al., 2008; M. Alenazy et al., 2021; L. Gómez-García et al., 2013; M. Borisova et al., 2017 Pro-inflammatory Serum; gene expression
IL-35 M. Alenazy et al., 2021 Anti-inflammatory Serum

Effects of abatacept on cytokine levels

IL-6 showed the most consistent and substantial reductions: IL-6 emerged as the cytokine with the most consistent and substantial reductions across studies. Following 24 weeks of abatacept treatment, IL-6 levels decreased significantly, representing an approximate 54% reduction. Changes in IL-6 levels correlated strongly with clinical improvement.

IL-17-producing T cells showed marked reductions, particularly in clinical responders: IL-17 demonstrated substantial reductions, showing a significant decrease particularly in clinical responders, normalizing to levels comparable with healthy controls.

IFN-γ showed moderate but significant reductions: IFN-γ demonstrated moderate reductions across multiple studies, particularly in cellular production.

Other pro-inflammatory cytokines showed variable responses: TNF-α showed only modest reductions. Additionally, cytokines such as IP-10 and Th1/Th2 cytokines (IL-2, IL-4, IL-10) showed decreases.

Anti-inflammatory cytokines increased with treatment: Uniquely, significant increases in anti-inflammatory cytokines IL-35 and IFN-β were reported.

Summary table of cytokine changes

Cytokine Study Baseline Post-treatment Change p-value
IL-6 M. Murakami et al., 2013 24.9±20.5 pg/mL 11.5±7.7 pg/mL (24 weeks) -54% <0.001
IL-6 M. Borisova et al., 2017 2.4 (1.1-6.4) pg/mL 1.29 (0.9-2.2) pg/mL (24 weeks) -46% 0.0006
IFN-γ (gene) M. Buch et al., 2008 Not specified Not specified -52% (95% CI -73 to -15) <0.05
IFN-γ (cellular) M. Scarsi et al., 2013a 70 (45-166) cells/μl 55 (43-82) cells/μl (6 months) -21.4% 0.036
IL-17 (cellular, CD4+) M. Scarsi et al., 2013a 19 (12-23) cells/μl 9 (4-16) cells/μl (6 months) -52.6% 0.017
IL-17 (% CD4+) M. Scarsi et al., 2013 1.1% (0.4-2.0) 0.3% (0.2-0.5) (12 months) -73% 0.005
IL-17 (% CD8+) M. Scarsi et al., 2013 1.2% (0.7-1.8) 1.0 (0.6-1.3) (6 months) -17% 0.035
IL-17 (serum) M. Alenazy et al., 2021 Not specified Not specified Decreased 0.0013
IP-10 M. Borisova et al., 2017 21 (12.9-49.8) pg/mL 14 (7.5-28) pg/mL (24 weeks) -33% 0.007
IL-22 M. Scarsi et al., 2014a 38.3 (7.7-93.0) pg/mL 33.8 (11.1-74.8) pg/mL (6 months) -12% 0.56 (NS)

Among pro-inflammatory cytokines, IL-6 demonstrated the most substantial and consistent decreases (46-54% reductions), followed by IL-17-producing cells (52.6-73% reductions in responders) and IFN-γ (21.4-52% reductions depending on measurement method). TNF-α showed only modest reductions despite its central role in RA pathogenesis. Anti-inflammatory cytokines IL-35 and IFN-β uniquely increased with treatment, suggesting abatacept may enhance regulatory mechanisms in addition to suppressing pro-inflammatory pathways.

References

M. Murakami, et al. (2013). Changes in Cytokine Profiles in Rheumatoid Arthritis Patients During Abatacept Treatment. Annals of the Rheumatic Diseases

M. Scarsi, et al. (2014). Reduction of peripheral blood T cells producing IFN-γ and IL-17 after therapy with abatacept for rheumatoid arthritis. Clinical and Experimental Rheumatology

M. Weisman, et al. (2006). Reduction of inflammatory biomarker response by abatacept in treatment of rheumatoid arthritis. Journal of Rheumatology

M. Buch, et al. (2008). Mode of action of abatacept in rheumatoid arthritis patients having failed tumour necrosis factor blockade: a histological, gene expression and dynamic magnetic resonance imaging pilot study. Annals of the Rheumatic Diseases

M. Scarsi, et al. (2013). Reduction of Peripheral Blood G-Ifn and IL-17 Producing T Cells After Therapy with Abatacept for Rheumatoid Arthritis. Annals of the Rheumatic Diseases

M. Alenazy, et al. (2021). Abatacept enhances blood regulatory B cells of rheumatoid arthritis patients to a level that associates with disease remittance. Scientific Reports

L. Gómez-García, et al. (2013). Reduced numbers of circulating CD28‐negative CD4+ cells in patients with rheumatoid arthritis chronically treated with abatacept. International Journal of Rheumatic Diseases

M. Borisova, et al. (2017). The effect of abatacept on cytokine profile in patients with rheumatoid arthritis. Annals of the Rheumatic Diseases

M. Scarsi, et al. (2014). IL-22 Levels after Abatacept Treatment in Rheumatoid Arthritis. Annals of the Rheumatic Diseases

M. Scarsi, et al. (2013). The effects of costimulation blockade performed by abatacept: Decreased production of G-IFN by CD8+ T cells and of IL-17 by CD4+ T cells after in vitro stimulation in good clinical responders. Annals of the Rheumatic Diseases