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Abstract Number: 1693

Innate, Adaptive, and TNF-Superfamily Immune Pathways Inform a Lupus Disease Activity Immune Index That Characterizes Disease Activity in SLE

Melissa E. Munroe1,2, Joel M. Guthridge1, Rufei Lu1,3, Joseph M. Kheir1, Bolanle Adebayo1, Susan R. Macwana1, Hua Chen1, Virginia C. Roberts1, Mohan Purushothaman2, Sanjiv Sharma2, Teresa Aberle1, Stan Kamp1, Cristina Arriens1, Eliza Chakravarty1, Katherine Thanou1, Joan T. Merrill1 and Judith A. James4,5, 1Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK, 2Progentec Diagnostics, Inc., Oklahoma City, OK, 3Medicine and Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 4University of Oklahoma Health Sciences Center, Oklahoma City, OK, 5Clinical Arthritis and Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK

Meeting: 2018 ACR/ARHP Annual Meeting

Keywords: autoantibodies, cytokines and systemic lupus erythematosus (SLE), Diagnostic Tests, Disease Activity

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Session Information

Date: Monday, October 22, 2018

Session Title: Systemic Lupus Erythematosus – Clinical Poster II: Biomarkers and Outcomes

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

Background/Purpose: Systemic lupus erythematosus (SLE) is a complex autoimmune disease marked by immune dysregulation. A comprehensive but cost-effective tool to track relevant mediators of altered disease activity would help improve disease management and prevent organ damage. The goal of this study was to identify critical components of a practical biometric to distinguish active from low lupus disease activity

Methods: SLE-linked immune mediators and autoantibodies were evaluated in 311 plasma samples from 198 patients with classified SLE procured on dates of low clinical disease (SLEDAI < 4, range 0-3, n=132) or more active disease (SLEDAI ≥ 4, range 4-30, n=179) as well as healthy controls (HC) matched for race, sex, and age (n=48). Thirty two soluble mediators and SLE-associated autoantibody specificities, including dsDNA, chromatin, Ro/SSA, La/SSB, Sm, SmRNP, and RNP, were assessed by multiplex bead-based assay or sandwich ELISA (BLyS, APRlL, and TGF-β). Soluble mediator levels were compared across clinical disease activity levels in conjunction with the presence of autoantibodies.

Results: Patients with low or active disease were similar in age, ethnicity, and sex. After adjusting for multiple comparisons (Bonferroni corrected p<0.0018), IL-6, IL-1α, IP-10, and IL-8 were significantly correlated with SLEDAI scores (Spearman r=0.179-0.253), yet 22/32 soluble mediators significantly correlated with the number of SLE-associated autoantibodies accrued, including those listed above, as well as SCF, IFN-α, IFN-γ, IL-17A, IL-10, MIG, MIP-1β, TNFRII, and BLyS (r=0.318 [IL-17A]-0.468 [IP-10]). The regulatory mediator IL-10 was highest in samples (p<0.05) from patients with low disease activity, while inflammatory mediators were highest in active disease samples with accrued autoantibody specificities (p<0.001). We integrated these findings to build a Lupus Disease Activity Immune Index (LDAII), calculated utilizing normalized (case vs. control) soluble mediator levels (n=32) weighted by the number of SLE-associated autoantibodies in each individual. The LDAII distinguished patients with clinically active (CA) vs. quiescent (CQ) disease who were either serologically (dsDNA binding and low complement) active (SA) or quiescent (SQ) (p<0.0001), whereby the number of accumulated autoantibodies (p<0.0001) as well as IL-6, IL-8, and IP-10 levels (p≤0.0006) were most significantly altered. In addition, the LDAII was able to differentiate clinically and serologically quiescent (CQSQ) SLE patients vs. HC (p=0.019). Finally, the LDAII significantly correlated with SLEDAI scores in patients (p<0.0001) and identified patients with renal organ involvement (p=0.002), in whom SCF, TNFRII, and MCP-1 were also most significantly altered (p≤0.005).

Conclusion: Clinically meaningful components of immunological profiles may help illuminate disease pathogenesis, guide therapy, improve clinical trial design, and detect serious autoimmune disease with subtle presentation.


Disclosure: M. E. Munroe, Progentec Diagnostics, Inc., 2; J. M. Guthridge, None; R. Lu, None; J. M. Kheir, None; B. Adebayo, None; S. R. Macwana, None; H. Chen, None; V. C. Roberts, None; M. Purushothaman, Progentec Diagnostics, Inc., 4; S. Sharma, Progentec Diagnostics, Inc., 4; T. Aberle, None; S. Kamp, None; C. Arriens, None; E. Chakravarty, None; K. Thanou, None; J. T. Merrill, None; J. A. James, None.

To cite this abstract in AMA style:

Munroe ME, Guthridge JM, Lu R, Kheir JM, Adebayo B, Macwana SR, Chen H, Roberts VC, Purushothaman M, Sharma S, Aberle T, Kamp S, Arriens C, Chakravarty E, Thanou K, Merrill JT, James JA. Innate, Adaptive, and TNF-Superfamily Immune Pathways Inform a Lupus Disease Activity Immune Index That Characterizes Disease Activity in SLE [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 10). https://acrabstracts.org/abstract/innate-adaptive-and-tnf-superfamily-immune-pathways-inform-a-lupus-disease-activity-immune-index-that-characterizes-disease-activity-in-sle/. Accessed January 28, 2021.
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