In addition, van Room and co-workers showed that T-cells taken from RA patients were able to react with human or self-Hsp60 and inhibit the activation of TNF-α (a pro-inflammatory factor) through the activation of Th2 cytokine regulator, whereas there were no regulatory effects observed in Hsp65 isolated from Mycobacterium tuberculosis [85,86]. This evidence concerns the gene HSPD1 and rheumatoid arthritis.