These complexes can deposit in tissues, initiating an inflammatory response and resulting in damage to multiple organs (46); (iii) The increased release of inflammatory mediators, such as type-I interferons (type-I IFN), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), contributes to the inflammatory processes and tissue damage associated with SLE (47); (iv) Circulating immune complexes (ICs) in the patient’s serum trigger the complement system, leading to the depletion of significant amounts of complements C3 and C4. Here, TNF is linked to systemic lupus erythematosus.