Table 2.
Class of therapy | Mechanism of action | Impact on macrophages | Side effects |
---|---|---|---|
Systemic therapy | |||
Corticosteroids | Inhibit arachidonic acid and IL-1 formation and thus produce both anti-inflammatory and immunosuppressive effect | Change macrophage phenotype toward M2 polarization (79) | Infection, hypertension, glaucoma, osteoporosis, avascular necrosis, hyperglycemia, myopathy, weight gain (86, 87) |
Immunosuppressants | cyclosporin A, | ||
Tacrolimus
IVIG |
Acts on T cells via calcineurin Acts on T cells via calcineurin Act on T and B cells, on interferon signaling pathway, and on defective elimination of immune complexes and other cellular debris |
Promote M1 to M2 macrophage phenotype switch when combined to mesenchymal stem cells (80). Protect macrophages from LPS/INFγ-mediated apoptosis (81). Favors M2-like phenotype (82, 83) promotes the inflammatory actions of M2-like macrophages and reduces the proinflammatory activities of M1-like macrophages (84, 85) |
Nephrotoxicity, cosmetic side effects (hypertrichosis, gingival hyperplasia) (88, 89) Nephrotoxicity, Neurotoxicity, diabetogenic, hypertension (90) Limited data, few reported adverse effects and mostly they are mild and transient. Severe reported adverse effects include Thromboembolic events and renal toxicity (91–94) |