Rheumatoid arthritis is a systemic autoimmune disease, characterized by chronic inflammation and damage to the joints. Immune dysregulation underlies the pathogenesis of rheumatoid arthritis, leading to uncontrolled production of antibodies, mainly rheumatoid factor and citrullinate, involved in the autoreactivity against cartilage and bone [117]. It is estimated that the prevalence of rheumatoid arthritis is around 1%, mainly in women [118]. The immunosuppressive effects of HCQ are due to the ability to modulate T-cell and B-cell hyperactivity, resulting in a reduction of pro-inflammatory cytokine gene expression. As the involvement of neutrophils in this disease, Jancinova, Pazourekova, Lucova, Perecko, Mihalova, Bauerova, Nosal and Drabikova [75] investigated the impact of oral HCQ administration on these cells, in rats with adjuvant arthritis. At doses of 40 mg/kg daily, per oral administration (p.o.), it strongly decreased the blood concentration of neutrophil-derived oxidants, involved in the tissue damage and the onset of chronic inflammation [75].