TNF-a and LT-a exert their pleiotropic functions by activating intracellular signaling cascades via binding to two types of receptors, TNFR-1 (encoded by the TNFRSF1A gene) and TNFR-2 (encoded by the TNFRSF1B gene) [30] . TNFR1deficient mice are resistant to endotoxic shock and have prolonged survival with less hypothermia [31] . TNFR2 influences the biological activity of TNF-a and LT-a both in a membranebound and a soluble form. Membrane-bound TNFR2 facilitates activation of nuclear factor (NF)-kB and mitogen-activated protein kinase signaling cascades upon binding with TNF-a and LT-a, whereas soluble TNFR2 is capable of binding and inactivating circulating TNF-a and LT-a [16, 30] . Moreover, animal studies showed that TNFR2 mediated protective effects in the development of severe sepsis [31] . Recent studies proposed that genetic variation in TNFRSF1A and TNFRSF1B was associated with susceptibility to inflammatory and autoimmune diseases, such as tuberculosis, systemic lupus erythematosus, rheumatoid arthritis and Crohn's disease [32, 33, 34, 35] . However, to date, only one study investigated the role of TNFRSF1A and TNFRSF1B polymorphisms in sepsis susceptibility and mortality [36] .