Impact of Retinoic Acid on Immune Cells and Inflammatory Diseases

Figure 3

Potential anti-inflammatory effects of RA. RA can decrease inflammatory processes, promoting homeostasis and attenuating harmful inflammatory responses in mucosa and tissues. RA shows immunosuppressive effect on Th1/Th17 cells in multiple sclerosis (MS) and induces Apo E in microglia, protecting from the neurotoxic effects mediated by amyloid β (Aβ) in Alzheimer disease (AD), contributing to neuronal homeostasis. RA is crucial for intestinal tolerance, by inducing Treg, cytokines IL-10 and IL-22, and antimicrobial peptide (AMP) synthesis, which may lead to Th17 inhibition. RA modulates inflammatory airway diseases (asthma and rhinitis) by inhibiting Th2/Th17 response and enhancing Treg cells. Retinoids increases type I collagen and TGF-β, reducing matrix metalloproteinase (MMPs) in photoaging (AGE), and reduces IL-1 family cytokines (IL-17 and TNF-α), IL-33, and epidermal hyperplasia in psoriatic (PSO) lesions. RA also has effects in adipocytes, promoting white adipose tissue (WAT) browning by differentiation into beige cells (antiobesity) instead of white cells (proobesity). The formation of brown adipocytes within WAT enhances energy expenditure and reduces obesity. In addition, RA can repress the expression of inflammatory chemokines and cytokines, inhibiting inflammatory responses triggered by obesity.