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Overactivation of the innate immune system together with the impaired downstream pathway of type I interferon-responding genes is a hallmark of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and systemic sclerosis (SSc). To date, limited data on the cross-disease innate gene signature exists among those diseases. We compared therefore an innate gene signature of Toll-like receptors (TLRs), seven key members of the interleukin (IL)1/IL1R family, and CXCL8/IL8 in peripheral blood mononuclear cells from well-defined patients with active stages of RA ( n  = 36, DAS28 ≥ 3.2), SLE ( n  = 28, SLEDAI > 6), and SSc ( n  = 22, revised EUSTAR index > 2.25). Emerging diversity and abundance of the innate signature in RA patients were detected: RA was characterized by the upregulation of  TLR3 ,  TLR5 ,  IL1RAP/IL1R3 ,  IL18R1 , and  SIGIRR/IL1R8  when compared to SSc ( P   corr  < 0.02) and of  TLR2 ,  TLR5 , and  SIGIRR/IL1R8  when compared to SLE ( P   corr  < 0.02). Applying the association rule analysis, six rules (combinations and expression of genes describing disease) were identified for RA (most frequently included high  TLR3  and/or  IL1RAP/IL1R3 ) and three rules for SLE (low  IL1RN  and  IL18R1 ) and SSc (low  TLR5  and  IL18R1 ). This first cross-disease study identified emerging heterogeneity in the innate signature of RA patients with many upregulated innate genes compared to that of SLE and SSc.

Cross-Disease Innate Gene Signature: Emerging Diversity and Abundance in RA Comparing to SLE and SSc