Table 1.
Targets, effect, and signaling pathways of biological disease-modifying anti-rheumatic drugs (bDMARDs).
| Treatment | Target | M1–M2 shift contribution | Signaling | Reference |
|---|---|---|---|---|
| CTLA4-Ig (abatacept) | CD80/CD86 | Downregulation of CD80, CD86, and TLR4 Upregulation of CD204, CD163 and CD206, MerTK |
Inhibition of NFkB | (42) (46) (47) |
| TNF inhibitors (infliximab, etanercept, adalimumab, golimumab and certolizumab) |
TNFα | Upregulation of IL-10, SOCS3, GAS6, CD16 |
Activation of STAT3 Inhibition of NFkB |
(100) |
| Rituximab | Anti-CD20 | Downregulation of CD40 | – | (100) |
| Tocilizumab | Anti-IL-6R | Downregulation of CD40 Upregulation of CD206 |
– | (100) |
Description of molecular targets, effect exerted on cells involved in the inflammatory process and signaling pathways modulated by biological disease-modifying anti-rheumatic drugs, such as CTLA4-Ig (abatacept), TNFα inhibitors (infliximab, etanercept, adalimumab, golimumab, certolizumab), anti-CD20 antibody (rituximab), and anti-IL-6 receptor antibody (anti-IL-6R, tocilizumab).
TLR4, toll-like receptor 4; CD204 and CD163, macrophage scavenger receptors; CD206, mannose receptor 1; MerTK, MER proto-oncogene, tyrosine kinase; TNF, tumor necrosis factor; IL-10, interleukine-10; SOCS3, suppressor of cytokine signaling 3; GAS6: growth arrest-specific 6; STAT3, signal transducer and activator of transcription 3.