We read with great interest the article written by Xia et al, which was recently published in Clinical Cardiology, reporting the involvement of programmed death (PD)-1 and its ligand B7 homologue (B7-H1) in the immunological response of patients with peripartum cardiomyopathy (PPCM). 1 The authors found that the expression of PD-1 and B7-H1 in peripheral blood lymphocytes was significantly lower in patients with PPCM compared to the control group. At the same time, they reported that the levels of interferon gamma (IFN-γ) were significantly elevated, and the levels of interleukin 4 (IL-4) were significantly reduced in PPCM patients compared to controls. 1 The authors found an inverse correlation between the PD-1 and B7-H1 expression and IFN-γ cytokine derived from type 1 T helper (Th1) lymphocytes, associated with cellular immune response, and at the same time a direct relationship between IL-4 levels, associated with humoral immune response generated by type 2 T helper (Th2) lymphocytes, and the enhanced expression of both PD-1 and B7-H1. Therefore, the study brings new and relevant insights into the pathogenesis of this disorder, which can be fatal in otherwise healthy young women, and the authors can be congratulated for their results.However, after carefully reading the article, we have several comments.Despite the relevant value of the observations reported, the findings of the study raise several questions that are not addressed in the article. The first derives from the fact that PPCM patients expressed decreased levels of IL-4, characterizing humoral immunity, and at the same time elevated levels of IFN-γ, characterizing cell immune response. This is exactly opposed to the normal immune response to pregnancy, which is to suppress the Th1 cells (cellular immunity) in favor of the Th2 immunity type (humoral immunity). 2,3 In our opinion, it would be interesting to discuss which of these 2 findings is responsible to a higher extent for the development of PPCM. Is it the augmented cellular immunity, the suppressed humoral immunity, or is it rather the imbalance between the 2? Can an enhanced cellular immunological response, expressed by an increased level of IFN-γ, trigger the onset of the disease, or is it the decrease of IL-4 (associated with humoral response) that leads to development and progression of PPCM? However, the exact dimension of the imbalance between the 2 types of immune responses in PPCM and their role in the pathogenesis of the disease is still unelucidated.The second issue, which is only partially addressed in the article, refers to the role of inflammatory cytokines in the pathogenesis of PPCM. PPCM is a disease characterized by progressive heart failure.Heart failure is associated with significant release of inflammatory cytokines in the peripheral blood, whereas PD-1 and B7-H1 depresses T helper cell-mediated immune reactivity through reducing secretion of multiple cytokines. In our opinion, it would be interesting to discuss whether the changes in cytokine pattern can trigger the onset...