In this study, 31 CF patients undergoing therapeutic treatments with Trikafta or Symkevi were enrolled, and monocytes from blood samples were isolated and analyzed. The results show that the therapy was able to correct the activation defect of the integrin LFA-1 (Lymphocyte function-associated antigen) for 23 out of 25 patients treated with Trikafta and for 5 out of 6 patients treated with Symkevi. The results of the experiments, therefore, confirmed the correlation between the defect on CFTR and the defective LFA-1 which leads to malfunction of monocytes and persistence of lung inflammation/infection. The researchers also report that therapeutic approaches to recover CFTR function have also improved the function of the defective monocytes as well.
The measurement of integrin activity could be used to evaluate the effectiveness of therapeutic treatments with CFTR modulators in CF patients.