Disease-Specific Autoantibodies Induce Trained Immunity in RA Synovial Tissues and Its Gene Signature Correlates with the Response to Clinical Therapy

<div>Schematic overview of <i>in vitro</i> trained immunity model by RA autoantibodies. Freshly isolated CD14+ human monocytes were cultured for 24 h in RPMI 1640 medium in Petri dishes precoated with 10 <i>μ</i>g/ml purified ACPA IgG (cACPA/IgG), RF IgM (cRF/IgM), or IVIG (cIgG). Control cells were cultured with RPMI 1640 medium or in the presence of LPS (1 <i>μ</i>g/ml). After priming, the monocytes were detached, washed, and subcultured in 96-well plates for resting. Then, the Mo(cACPA/IgG), Mo(cRF/IgM), Mo(cIgG), Mo(control), and Mo(LPS) were stimulated by LPS (10 ng/ml) for 24 h. Cytokines and chemokines in the supernatants from either the priming or stimulation phase were measured by ELISA.</div>

Mediators of Inflammation

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Figure 1

Figure 1: Disease-Specific Autoantibodies Induce Trained Immunity in RA Synovial Tissues and Its Gene Signature Correlates with the Response to Clinical Therapy 

Figure 1 | Disease-Specific Autoantibodies Induce Trained Immunity in RA Synovial Tissues and Its Gene Signature Correlates with the Response to Clinical Therapy 