Another remarkable result of our study is the decrease in CD86 expression by monocytes and DC after CRT compared to the initial evaluation, suggesting an immune modulating role of CRT, whether in responder or non-responder patients, due to a lower ability of monocytes and DC to provide the second antigen-independent co-signal to T cells, which may compromise the adaptive immune response on the inflammatory process in HF. This evidence concerns the gene CD86 and hydrops fetalis.