Polymorphonuclear leucocytes (PMNLs) represent the first line of defence in innate immunity. PMNLs are the predominant cells accumulating in the synovial fluid of rheumatoid arthritis (RA) patients and play a crucial role in the development of tissue damage. Unstimulated PMNLs are postmitotic terminally differentiated cells whose default setting is death by apoptosis. Pathogens or inflammation induce a profound transcriptional and translational activity. Aberrant expression of members of the major chaperone family HSP70 occurs in synovial tissue of RA [1, 2] and in PMNLs subjected to stress in the form of exercise  or polytrauma . Activity and substrate specificity of HSP70s is regulated by the family of J-proteins. HSP70s and J-proteins together generate important chaperone machines, which are not only involved in classical chaperone tasks like proper protein folding but also in fine tuning of molecules involved in signal transduction and apoptotic pathways. Hardly any data exist on J-protein expression in PMNLs.