Introduction
Organ failure (OF), as a general term, can be defined as impairment of vital functions of organ systems that are essential to the maintenance of life1. The common causes are as follows: Severe trauma, Severe infection, Major surgical operations, Various types of shock, Cardiac arrest2. The severity of organ dysfunction can be quantified according to the parameters that best define the major functions of a particular organ, such as partial pressure of arterial oxygen (PaO2) for pulmonary function or serum creatinine for renal function. Published data have showed that the serum sST2 levels were considered as independently predict all-cause mortality in patients with chronic heart failure3. However, the role of sST2 in OF patients remains unclear.
Suppression of tumorigensis-2 (ST2) is a member of the interleukin (IL)-1 receptor family4,5, with four protein isoforms identified to date. The two main isoforms are a transmembrane receptor ST2L and a soluble ST2 isoform (sST2)6,7. IL-33 binds to ST2L and activates mitogen-activated protein kinases (MAPK) and several biochemical pathways8,9. However, sST2 avidly binds IL-33, which results in interruption of the interaction between IL-33/ST2L; thus, sST2 is viewed as a decoy receptor, preventing transduction of favorable effects of IL-33 through ST2L10. Serum sST2 has been used as a biomarker for predicting heart failure, whether ST2 can be used as a screening indicator for other OF, or whether it can be combined with other related indicators to screen for OF.
CD4+T cells play a vital role in the adaptive immune response and are involved in the pathogenesis of many diseases11, including autoimmune diseases12, cancer13, and chronic inflammation14. As a major arm of the cellular immune response, CD4+T cells can be classified as Th1 (T-bet and IFN-γ), Th2 (GATA3 and IL-4/IL-13), Th17 (ROR-γt and IL-17), Tfh (Bcl6 and IL-21) and Treg (Foxp3 and IL-10/IL-35) according to the expression of characteristic cytokines and their lineage-specific transcription factors15,16. As a highly heterogeneous population of cells, it is not clear whether they are involved in the development of OF.
Therefore, the present work was to address the above question; our results showed that serum sST2 levels were significantly up-regulated in OF patients and peripheral blood CD4+T cells significantly decreased with the increase of sST2. The present work revealed a novel role and phenomenon of sST2: Serum sST2 level was obviously correlated with the number of CD4+T cells in OF patients.