CTLA4 and asthma: For example, miR-181b-5p is lowly expressed in airway epithelial tissue and plasma of asthma patients, and it can inhibit the expression of proinflammatory cytokines by targeting SPP1, thus participating in the inhibition of eosinophilic airway inflammation [10]; miR-155 improves the viability of Th cells by down-regulating CTLA-4 expressions, thus inducing asthma [11].