J. P. Cobb

TL;DR: It is concluded that caspase-3-mediated apoptosis causes extensive lymphocyte apoptosis in sepsis and may contribute to the impaired immune response that characterizes the disorder.

TL;DR: It is shown that critical injury in humans induces a genomic storm with simultaneous changes in expression of innate and adaptive immunity genes that alter the status of these genes in the immune system.

TL;DR: Although there was no overall effect on lymphocytes from critically ill nonseptic patients (considered as a group), certain individual patients did exhibit significant loss of B and CD4 T cells in sepsis, which is especially significant because it occurs during life-threatening infection, a state in which massive lymphocyte clonal expansion should exist.

TL;DR: These two studies employing different methods of blocking lymphocyte apoptosis provide compelling evidence that immunodepression resulting from the loss of lymphocytes is a central pathogenic event in sepsis, and they challenge the current paradigm that regardssepsis as a disorder resulting from an uncontrolled inflammatory response.

TL;DR: It is concluded that overexpression of Bcl-2 provides protection against cell death in sepsis, which may be beneficial by down-regulating the accompanying inflammation and detrimental by compromising host defense.