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J. Biol. Chem., Vol. 277, Issue 42, 39320-39326, October 18, 2002
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From the Aspergillus fumigatus causes
life-threatening infections in patients with qualitative and
quantitative defects in phagocytic function. Here, we examined the
contribution of Toll-like receptor (TLR)-2, TLR4, the adapter protein
MyD88, and CD14 to signaling in response to the three forms of A. fumigatus encountered during human disease: resting conidia (RC),
swollen conidia (SC), and hyphae (H). Compared with elicited peritoneal
macrophages obtained from wild-type and heterozygous mice,
TLR2
Toll-like Receptor (TLR) Signaling in Response to
Aspergillus fumigatus*
§,,
**
Evans Memorial Department of Clinical
Research, Departments of Medicine and Microbiology, Boston
University School of Medicine, Boston, Massachusetts 02118 and the
¶ Department of Medicine, University of Massachusetts Medical
School, Worcester, Massachusetts 01605
/ and MyD88/ macrophages produced
significantly less tumor necrosis factor-
(TNF) following
A. fumigatus stimulation. In contrast, following stimulation with RC, SC, and H, TLR4/ and
CD14/ macrophages exhibited no defects in tumor
necrosis factor- release. TLR2/,
TLR4/, MyD88/, and
CD14/ macrophages bound similar numbers of RC and SC
compared with wild-type macrophages. RC, SC, and H stimulated
greater activation of a nuclear factor 
B
(NFB)-dependent reporter gene and greater release of
tumor necrosis factor- from the human monocytic THP-1 cell
line stably transfected with CD14 compared with control cells stably
transfected with empty vector. A. fumigatus stimulated NFB-dependent reporter gene activity in the human
embryonic kidney cell line, HEK293, only if the cells were transfected
with TLR2. Moreover, activity increased when TLR2 and CD14 were
co-transfected. Taken together, these data suggest that optimal
signaling responses to A. fumigatus require TLR2 in both
mouse and human cells. In contrast, a role for CD14 was found only in
the human cells. MyD88 acts as a central adapter protein mediating
signaling responses following stimulation with RC, SC, and H.
*
This work was supported in part by National Institutes of
Health Grants AI-37532, AI-25780, RR14466, GM54060, DK50305, and HL07501.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Recipient of a Burroughs Wellcome Fund Scholar Award in
Pathogenic Mycology.
**
To whom correspondence should be addressed: Rm. X626, Boston
Medical Center, 650 Albany St., Boston, MA 02118. Tel.: 617-638-7904; Fax: 617-638-7923; E-mail: slevitz@bu.edu.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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