tion with compounds targeting LXR could additional modulate lipid rafts and AIRD drug efficacies remains to be explored. In some circumstances, the dose of lipid-modifying therapies must be adjusted when they are utilised in mixture with AIRD therapies. Tocilizumab normalizes CYP enzyme expression and increases LDL-C; as a result patients on statin cotherapy may require an VEGFR3/Flt-4 custom synthesis enhanced dose to maintain therapeutic lipid-lowering positive aspects (135). Cyclosporin also can affect the pharmacokinetics of statins via the inhibition of each organic anion transporter polypeptide-1B1 and CYP3A4 (178). Also, lipids like HDL play an important role as S1P chaperones; therefore, alterations in lipoprotein metabolism could influence the efficacy of drugs modulating the S1P pathway (e.g., fingolimod), that are now employed in various sclerosis and becoming investigated in AIRDs (34, 179).R E V I E W S E R I E S : I M M U N O M E TA B O L I S MDietary patterns also modify inflammation; those with a larger inflammatory potential are significantly linked with unfavorable lipid profiles along with a greater incidence of CVD (180). Despite these observations, the relationship involving nutrition and inflammation in AIRDs will not be nicely established. Oral lipid supplements may possibly help the effectiveness of conventional therapies, for instance important fatty acid supplementation to enhance STM levels; these have been linked to decreased joint pain and predict DMARD responsiveness in RA (31). Dietary polyunsaturated fatty acids can also inhibit ferroptosis (181) and incorporate into T cell membranes, thus altering plasma membrane phospholipid expression plus the localization of immunogenic receptors like IL-2 receptor and Fc receptors into lipid raft microdomains (182). Dietary intervention to alter blood lipids may be useful in SLE and RA and minimize illness activity scores (18385). Improved dietary intake of omega-3 fatty acids improved HDL and lowered triglycerides in juvenile-onset SLE (183, 186) and increased HDL and reduced VLDL in adult SLE (187). Hence omega-3 dietary supplements may be promising therapeutic selections for some patients. In contrast, a randomized controlled trial of dietary restrictive patterns lowered weight and fatigue in adults with SLE, but did not have an effect on disease activity or cardiovascular parameters such as lipid profiles and inflammatory markers (188).ConclusionUnderstanding how lipid metabolism influences immune responses plus the effect of each standard and new therapies on lipid metabolism is an ongoing challenge but could Toxoplasma Species determine new methods to target AIRDs. Far better control of inflammation applying optimal combinations of immunosuppressive treatments, as shown in inflammatory bowel illness (189), could lead to an enhanced metabolic/ lipid profile in AIRDs. Improved monitoring of pro-/antiinflammatory lipoprotein fractions utilizing a granular lipoprotein taxonomy method and improved CVD threat stratification biomarkers (171, 172), instead of total HDL/LDL levels, could strengthen targeted patient management. This can be relevant given that statins do not fully normalize proinflammatory HDL fractions (160). Such improved monitoring could enable novel mixture interventions, for instance nonspecific dietary intervention with particular lipid lowering and targeted antiinflammatory therapy. Lastly, the clinical relevance of metabolic/lipid biomarkers in AIRDs needs to become explored in longterm studies to capture the long-term toxicity of combined therapies at the same time