HSP60 participates in many interactions between the system integrated by all chaperones and closely associated molecules (chaperoning system or CS) and the immune system (IS). These interactions occur constantly to maintain normal cell physiology but, occasionally, they are perturbed and become mediators of pathologic events that may lead to disease. This switch to pathology may be initiated by various factors, genetic or acquired, which cause qualitative and/or quantitative modifications of HSP60, or immune crossreactivity between the human and microbial chaperonin orthologs, or a break in the balance between the pro- and anti-inflammatory actions of the chaperonin. Thus, autoimmune and chronic inflammatory pathologies may occur. Likewise, a perturbation of the CS-IS interactions, e.g., those that take place during ageing, may favor carcinogenesis. HSP60 may be commandeered by tumor cells to assist its high-rate protein synthesis and, also, to be an emissary among the devices tumor cells utilize to avoid anti-tumor immune reactions. Here, we briefly discuss the canonical and non-canonical functions of HSP/chaperones; and HSP60 as a multifunctional molecule, its migration itinerary, and its possible roles during carcinogenesis and in certain chronic inflammatory and autoimmune diseases. We examine the potential of HSP60 as a biomarker useful for diagnosing and monitoring the progression of the various conditions in which it actively participates. Lastly, we discuss the use HSP60 as target for controlling its activity when it is an etiopathogenic factor, or as a therapeutic agent to correct its deficiency.
|Numero di pagine||12|
|Rivista||CURRENT IMMUNOLOGY REVIEW|
|Stato di pubblicazione||Published - 2017|