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.