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Novel Signal Transduction Pathway Utilized by Extracellular
HSP70
ROLE OF Toll-LIKE RECEPTOR (TLR) 2 AND TLR4*
Alexzander
Asea,
Michael
Rehli§,
Edith
Kabingu,
Jason A.
Boch¶,
Olivia
Baré,
Philip E.
Auron¶,
Mary Ann
Stevenson, and
Stuart K.
Calderwood**
From the Department of Radiation Oncology,
Dana-Farber Cancer Institute, Harvard Medical School, Boston,
Massachusetts 02115, the § Department of Hematology and
Oncology, University of Regensburg Medical Hospital, Regensburg 93042, Germany, the ¶ Department of Medicine, Harvard Medical School and
New England Baptist Bone and Joint Institute, Beth Israel Deaconess
Medical Center, Boston, Massachusetts 02115, and the Department
of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard
Medical School, Boston, Massachusetts 02115
Recent studies have initiated a paradigm shift in
the understanding of the function of heat shock proteins (HSP). It is
nowclear that HSP can and do exit mammalian cells, interact withcells
of the immune system, and exert immunoregulatory effects.We recently
demonstrated that exogenously added HSP70 possessespotent cytokine
activity, with the ability to bind with high affinityto the plasma
membrane, elicit a rapid intracellular Ca2+ flux,
activate NF-B, and up-regulate the expression of pro-inflammatorycytokines in human monocytes. Here for the first time, we reportthat
HSP70-induced proinflammatory cytokine production is mediatedvia the
MyD88/IRAK/NF-B signal transduction pathway and thatHSP70 utilizes
both TLR2 (receptor for Gram-positive bacteria)and TLR4 (receptor for
Gram-negative bacteria) to transduce itsproinflammatory signal in a
CD14-dependent fashion. These studiesnow pave the way for
the development of highly effective pharmacologicalor molecular tools
that will either up-regulate or suppress HSP70-inducedfunctions in
conditions where HSP70 effects are desirable (cancer)or disorders
where HSP70 effects are undesirable (arthritis andarteriosclerosis).
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177, 7184-7192
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Heat Shock Treatment of Tumor Lysate-Pulsed Dendritic Cells Enhances Their Capacity to Elicit Antitumor T Cell Responses against Medullary Thyroid Carcinoma.
T. Bachleitner-Hofmann, M. Strohschneider, P. Krieger, M. Sachet, P. Dubsky, H. Hayden, S. F. Schoppmann, R. Pfragner, M. Gnant, J. Friedl, et al. (2006)
J. Clin. Endocrinol. Metab.
91, 4571-4577
|Abstract »|Full Text »|PDF »
Heat shock proteins induce T cell regulation of chronic inflammation.
F Hauet-Broere, L Wieten, T Guichelaar, S Berlo, R van der Zee, and W Van Eden (2006)
Ann Rheum Dis
65, iii65-iii68
|Abstract »|Full Text »|PDF »
Insulin induces myocardial protection and Hsp70 localization to plasma membranes in rat hearts.
G. Li, I. S. Ali, and R. W. Currie (2006)
Am J Physiol Heart Circ Physiol
291, H1709-H1721
|Abstract »|Full Text »|PDF »
Killing of Normal Melanocytes, Combined with Heat Shock Protein 70 and CD40L Expression, Cures Large Established Melanomas.
L. Sanchez-Perez, T. Kottke, G. A. Daniels, R. M. Diaz, J. Thompson, J. Pulido, A. Melcher, and R. G. Vile (2006)
J. Immunol.
177, 4168-4177
|Abstract »|Full Text »|PDF »
Extracellular heat shock protein 72 is a marker of the stress protein response in acute lung injury.
M. T. Ganter, L. B. Ware, M. Howard, J. Roux, B. Gartland, M. A. Matthay, M. Fleshner, and J.-F. Pittet (2006)
Am J Physiol Lung Cell Mol Physiol
291, L354-L361
|Abstract »|Full Text »|PDF »
Interaction of TLR2 and TLR4 Ligands with the N-terminal Domain of Gp96 Amplifies Innate and Adaptive Immune Responses.
T. Warger, N. Hilf, G. Rechtsteiner, P. Haselmayer, D. M. Carrick, H. Jonuleit, P. von Landenberg, H.-G. Rammensee, C. V. Nicchitta, M. P. Radsak, et al. (2006)
J. Biol. Chem.
281, 22545-22553
|Abstract »|Full Text »|PDF »
Invited review: Roles for accessory molecules in microbial recognition by Toll-like receptors.
K. Miyake (2006)
Innate Immunity
12, 195-204
|Abstract »|PDF »
Extracellular Targeting of Endoplasmic Reticulum Chaperone Glucose-Regulated Protein 170 Enhances Tumor Immunity to a Poorly Immunogenic Melanoma.
X.-Y. Wang, H. Arnouk, X. Chen, L. Kazim, E. A. Repasky, and J. R. Subjeck (2006)
J. Immunol.
177, 1543-1551
|Abstract »|Full Text »|PDF »
High-Affinity Interactions between Peptides and Heat Shock Protein 70 Augment CD8+ T Lymphocyte Immune Responses.
J. B. Flechtner, K. P. Cohane, S. Mehta, P. Slusarewicz, A. K. Leonard, B. H. Barber, D. L. Levey, and S. Andjelic (2006)
J. Immunol.
177, 1017-1027
|Abstract »|Full Text »|PDF »
Inhibition of Toll-like Receptor 4 With Eritoran Attenuates Myocardial Ischemia-Reperfusion Injury.
A. Shimamoto, A. J. Chong, M. Yada, S. Shomura, H. Takayama, A. J. Fleisig, M. L. Agnew, C. R. Hampton, C. L. Rothnie, D. J. Spring, et al. (2006)
Circulation
114, I-270-I-274
|Abstract »|Full Text »|PDF »
Stress Wars: the Direct Role of Host and Bacterial Molecular Chaperones in Bacterial Infection.
B. Henderson, E. Allan, and A. R. M. Coates (2006)
Infect. Immun.
74, 3693-3706
|Full Text »|PDF »
The role of human glioma-infiltrating microglia/macrophages in mediating antitumor immune responses.
S. F. Hussain, D. Yang, D. Suki, K. Aldape, E. Grimm, and A. B. Heimberger (2006)
Neuro Oncology
8, 261-279
|Abstract »|Full Text »|PDF »
,
, and
B, and up-regulate the expression of pro-inflammatory cytokines in human monocytes. Here for the first time, we report that
HSP70-induced proinflammatory cytokine production is mediated via the
MyD88/IRAK/NF-
