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Blood, 15 October 2003, Vol. 102, No. 8, pp. 2910-2915.
Prepublished online as a Blood First Edition Paper on June 26, 2003; DOI 10.1182/blood-2003-03-0967.
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IMMUNOBIOLOGY
A caspaselike activity is triggered by LPS and is required for survival of human dendritic cells
Luigi Franchi,
Ivano Condò,
Barbara Tomassini,
Chiara Nicolò, and
Roberto Testi
From the Laboratory of Immunology and Signal Transduction, Department of Experimental Medicine and Biochemical Sciences, University of Rome "Tor Vergata," Rome, Italy.
Bacterial endotoxin (lipopolysaccharide [LPS]) is a potent inducer of human dendritic cell (DC) maturation and survival. Here we show that immature DCs exposed to LPS trigger an early and sustained caspaselike activity, which can be blocked by zVAD (z-Val-Ala-Asp), in the absence of detectable caspase 8 and caspase 10 activation, or poly(ADP-ribose) polymerase (PARP)–cleaving activity. Preventing LPS-induced caspaselike activation in DC results in massive cell death. Importantly, triggering of the caspaselike activity is required for LPS-induced activation of extracellular signal-regulated kinases (ERKs) and for LPS-induced up-regulation of cFLIP (Fas-associating protein with death domain–like interleukin-1 –converting enzyme [FLICE]–like inhibitory protein). Therefore, a caspase-dependent pathway initiated by LPS controls survival of human DCs.
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