Cytheris SA, a clinical stage biopharmaceutical company focused on
research and development of new therapies for immune modulation, today
announced publication of data from a preclinical study in a clinically
relevant animal model of sepsis showing that recombinant human
Interleukin-7 (rhIL-7) treatment not only restores T cell trafficking
and function, but also translates into improved survival. Sepsis, a
highly lethal disorder which occurs during severe overwhelming
infection, is the most common cause of death in most intensive care
units in developed countries, annually striking an estimated 750,000
people in the United States alone, resulting in the death of more than
220,000 people per year.
“IL-7 Promotes T Cell Viability, Trafficking, and
Functionality and Improves Survival in Sepsis”
The paper entitled “IL-7 Promotes T Cell Viability, Trafficking, and
Functionality and Improves Survival in Sepsis” is prepublished online in The
Journal of Immunology, the journal of The American Association of
Immunologists (Jacqueline Unsinger, Margaret McGlynn, Kevin R. Kasten,
Andrew S. Hoekzema, Eizo Watanabe, Jared T. Muenzer, Jacquelyn S.
McDonough, Johannes Tschoep, Thomas A. Ferguson, Jonathan E. McDunn,
Michel Morre, David A. Hildeman, Charles C. Caldwell, and Richard S.
Hotchkiss, March 3, 2010; doi:10.4049/jimmunol.0903151).
The study strongly supports the belief that rather than being an
uncontrolled inflammatory response, sepsis is the result of extensive
apoptosis-induced depletion of immune effector cells. This explains the
failure of the numerous sepsis trials conducted with agents that block
the inflammatory cascade, leading investigators to question whether
death in patients with sepsis results from uncontrolled inflammation.
Three autopsy studies of patients who died of sepsis have confirmed
findings in animal models by showing massive loss of T and B lymphocytes
and dendritic cells.
“Based on this study, rhIL-7 appears to be a particularly attractive
therapy for this indication because it ameliorates many of the key
pathophysiologic processes that are believed to be central to the
lethality of sepsis,” said Richard S. Hotchkiss, MD, Department of
Anesthesiology, Washington University School of Medicine and lead
investigator on the study. “Specifically, rhIL-7 blocks sepsis-induced
depletion of CD4 and CD8 cells, enhances lymphocyte recruitment,
prevents the sepsis-induced loss in immunity as evidenced by preserved
delayed-type hypersensitivity response, does not exacerbate the
proinflammatory response in sepsis, and clearly improves survival.”