Although rhCC16 treatment did not reduce PD-1 or Tim-3 expression on T or B lymphocytes, or NK cells in CS-exposed WT or Cc16–/– lungs, future studies should investigate the contributions of CC16 to adaptive immunity and immune tolerance/exhaustion in murine models of COPD exacerbations. This evidence concerns the gene PDCD1 and chronic obstructive pulmonary disease.