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Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia
Correspondence: K. Murali Krishna Rao, M.D., Box 2015, PPRB/HELD/NIOSH, 1095 Willowdale Road, Morgantown, WV 26505. E-mail: mir8{at}cdc.gov
Stimulation of macrophages by a variety of agents causes activation of
mitogen-activated protein kinases (MAPKs). Activation of MAPKs by
lipopolysaccharide involves CD14 and Toll receptors. Subsequent steps
still remain to be explored. Tumor necrosis factor-
(TNF-)-induced activation of MAPKs has been shown to involve the
death domain proteins (TRADD, FADD, MADD) and TRAFs. Other molecules
involved in this pathway include the protein kinases, ASK1, germinal
center kinase (GCK), hematopoietic progenitor kinase 1 (HPK1), and
GCK-related kinase (GCKR). Although, these pathways have been described
in various cell types, their role in macrophages remains to be
established. The availability of knockout mice and constitutively
active and dominant-negative mutants of MAPKs should greatly enhance
our understanding of this field. The activation of MAPKs seems to be
different in cell lines compared with primary cells. Among the
macrophages, cells from different compartments show different
expression of receptors and signal transduction molecules. These
differences may account for differences in MAPK activation and other
phenotypic differences in macrophages from different compartments.
Therefore, it is important to use primary cells for studying MAPK
signal-transduction pathways, and the data from cell lines should not
be extrapolated to primary cells.
Key Words: Toll • TNF • TRAF • CD14 • GCK
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