Induction of heat shock proteins in B-cell exosomes
Author:
Clayton Aled1, Turkes Attilla1, Navabi Hossein1, Mason Malcolm D.1, Tabi Zsuzsanna1
Affiliation:
1. Department of Clinical Oncology and Palliative Medicine, Wales College of Medicine, Cardiff University, Velindre Cancer Centre, Whitchurch, Cardiff, CF14 2TL, UK
Abstract
Exosomes are nanometer-sized vesicles secreted by a diverse range of live cells that probably have physiological roles in modulating cellular immunity. The extracellular factors that regulate the quantity and phenotype of exosomes produced are poorly understood, and the properties of exosomes that dictate their immune functions are not yet clear.
We investigated the effect of cellular stress on the exosomes produced by B-lymphoblastoid cell lines. Under steady-state conditions, the exosomes were positive for hsp27, hsc70, hsp70 and hsp90, and other recognised exosome markers such as MHC class I, CD81, and LAMP-2. Exposing cells to heat stress (42°C for up to 3 hours), resulted in a marked increase in these heat shock proteins (hsps), while the expression of other stress proteins such as hsp60 and gp96 remained negative, and other exosome markers remained unchanged. Stress also triggered a small increase in the quantity of exosomes produced [with a ratio of 1.245±0.07 to 1 (mean±s.e.m., n=20) of 3-hour-stress-exosomes to control-exosomes]. Flow-cytometric analysis of exosome-coated beads and immuno-precipitation of intact exosomes demonstrated that hsps were located within the exosome lumen, and not present at the exosome-surface, suggesting that such exosomes may not interact with target cells through cell-surface hsp-receptors. Functional studies further supported this finding, in that exosomes from control or heat-stressed B cells did not trigger dendritic cell maturation, assessed by analysis of dendritic-cell-surface phenotype, and cytokine secretion profile.
Our findings demonstrate that specific alterations in exosome phenotype are a hitherto unknown component of the cellular response to environmental stress and their extracellular function does not involve the direct activation of dendritic cells.
Publisher
The Company of Biologists
Reference42 articles.
1. Altieri, S., Khan, A. and Tomasi, T. (2004). Exosomes from Plasmacytoma cells as a tumor vaccine. J. Immunother.27, 282-288. 2. Andre, F., Schartz, N. E., Movassagh, M., Flament, C., Pautier, P., Morice,
P., Pomel, C., Lhomme, C., Escudier, B., Le Chevalier, T. et al. (2002). Malignant effusions and immunogenic tumour-derived exosomes. Lancet360, 295-305. 3. Bard, M. P., Hegmans, J. P., Hemmes, A., Luider, T. M., Willemsen, R.,
Severijnen, L.-A. A., Meerbeeck, J. P. V., Burgers, S. A., Hoogsteden, H. C. and Lambrecht, B. N. (2004). Proteomic analysis of exosomes isolated from human malignant pleural effusions. Am. J. Respir. Cell. Mol. Biol.31, 114-121. 4. Basu, S., Binder, R. J., Suto, R., Anderson, K. M. and Srivastava, P. K. (2000). Necrotic but not apoptotic cell death releases heat shock proteins, which deliver a partial maturation signal to dendritic cells and activate the NF-kappa B pathway. Int. Immunol.12, 1539-1546. 5. Basu, S., Binder, R. J., Ramalingam, T. and Srivastava, P. K. (2001). CD91 is a common receptor for heat shock proteins gp96, hsp90, hsp70, and calreticulin. Immunity14, 303-313.
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