Expression of programmed cell death-1 and its ligand B7 homolog 1 in peripheral blood lymphocytes from patients with peripartum cardiomyopathy

Background: Immune response has been postulated to play a prominent role in the pathogenesis of peripartum cardiomyopathy (PPCM). Given the importance of programmed death (PD)-1 and its ligand B7 homologue 1 (B7-H1) costimulatory molecules as an immune regulatory pathway, this study aimed to investigate the effect of PD-1 and B7-H1 expression on immune response in peripheral blood lymphocytes from the patients with PPCM. Hypothesis: PD-1 and B7-H1 may be involved in modulating immune response in PPCM. Methods: Peripheral blood lymphocytes were obtained from PPCM and pregnancy-matched healthy women. PD-1 and B7-H1 expression were determined using fluorescence quantitative reverse transcription-polymerase chain reactions (RT-PCR) and Western blot. The presence of serum interferon (IFN)-γ and interleukin (IL)-4 were determined with enzyme-linked immunosorbent assay. Results: The levels of pro-brain natriuretic peptide and IFN-γ were markedly elevated, whereas the levels of left ventricular ejection fraction and IL-4 were significantly reduced in PPCM patients compared to controls. Additionally, both RT-PCR and Western blot revealed that the levels of PD-1 and B7-H1 expression were decreased significantly in PPCM patients compared with controls. A significant positive correlation was observed between PD-1 and B7-H1 expression. Furthermore, PD-1 and B7-H1 expression showed significant negative correlation with IFN-γ, as well as positive correlation with IL-4. Therefore, decreased expression of PD-1 and B7-H1 led to a dysregulating immune response such that cellular immunity linked to T helper (Th)1 cells was predominant over humoral immunity linked to Th2 cells in PPCM. Conclusions: This study provided the first findings that PD-1 and B7-H1 expression were decreased, which might impair functional regulation of negative costimulation on immune response that may work in the etiopathogenesis of PPCM.