Extracellular Heat Shock Proteins as Regulator of the Immune System

Dear Colleagues,

Heat shock proteins (HSPs) were first described in 1962 as temperature-sensitive proteins in Drosophila. HSPs have mainly been studied as intracellular proteins, helping other proteins to maintain their structure and function under stress conditions, including physiological stress, mechanical stress, environmental stress (heat, cold, UV-light), and infections. In 1991, it was reported that extracellular HSPs activate gamma-delta T-lymphocytes.

The HSPs of microorganisms such as Chlamydia induce the formation of antibodies to human HSPs, leading to an auto-immune reaction, which is associated with the chronic inflammation observed in rheumatic disorders, cardiovascular diseases and others.

Circulating HSP60 has been linked to increased pro-inflammatory cytokine levels in patients with coronary heart diseases, and obesity. In contrast, circulating HSP70 protected against cardiovascular disease. However, serum HSP70 correlated with chronic glomerulonephritis, and hepatic dysfunction.

The contribution of extracellular HSPs to health and disease is not well understood and requires further investigation. The action of extracellular HSPs is most likely modified by the presence of anti-HSP antibodies, and the ratio between these two factors and their consequences in chronic inflammatory diseases remains incompletely understood.

Therefore, we are collecting manuscripts investigating the function and signal mediation pathways of extracellular HSPs and anti-HSP antibodies in the context of chronic inflammation.

Prof. Dr. Michael Roth
Guest Editor
Dr. Fang Lei
Co-Guest Editor

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