Increased apoptosis of alveolar lymphocytes (AL) in idiopathic pulmonary fibrosis (IPF). Potential mechanisms and practical considerations

Background: The implication of T cells in IPF pathogenesis is controversial. The views vary from direct lymphocytes participation in lung fibrosis to their protective role against the process. Aim: Examination of AL apoptosis frequency in IPF. Results were related to clinical data and BAL cytoimmunological pattern, in order to evaluate the physiopathological role of AL and T cell apoptosis mechanisms in IPF. Methods. BAL of 27 IPF patients and 17 controls was examined for: a) cytoimmunology, b) supernatant levels of cytokines taking part in cell apoptosis/survival (ELISA), c) AL apoptosis with flow cytometry (sub-G1 peak of cell cycle); d) TUNEL assay; e) AL staining for BCL-2, BCL-xL, BAK, caspase-3, and death receptors (DRs). Results. In all methods AL apoptosis was higher in IPF than in controls (sub-G1 peak: 2.8±2.2 vs 1.0±0,2%, p Conclusions. AL protect lung tissue from fibrosis; AL apoptosis is an unfavourable process and its inhibition should be considered as important therapeutic option in IPF. Its mechanisms may include BCL-2 family proteins interaction, and TNFα:TNFR1 ligation. The way that neutrophiles impact AL apoptosis needs further explanation.