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. 2016 Jun 13;7:203. doi: 10.3389/fimmu.2016.00203

Figure 1.

Figure 1

Induction and regulation of adjuvant arthritis by immune response to Hsp65. AA can be induced in Lewis rats by subcutaneous immunization with heat-killed M. tuberculosis H37Ra (Mtb). Mycobacterial hsp65 (Bhsp5) is one of the targets of immune response in arthritic rats. The T cells against epitope 180–188 of Bhsp65 (B180) are pathogenic, whereas those against other epitopes of Bhsp65 [e.g., 256–270 (B256) and Bhsp65 C-terminal determinants (BCTD)] are regulatory in AA. Tolerization of rats with soluble Bhsp65 or B180 renders these rats relatively resistant to induction of AA by subsequent Mtb injection. Arthritic rats also raise antibody response to Bhsp65, and antibodies have been shown to be protective against AA. Intriguingly, immunization of Lewis rats with self-Hsp65 [e.g., human Hsp60 or rat Hsp65 (Rhsp65)] is protective rather than pathogenic. Similarly, induction of antibody response by a peptide of self-Hsp60 also affords protection against AA. Finally, challenge with altered peptide ligands (APLs) of Bhsp65 and self-Hsp60 can induce a disease-protective response in arthritic rats. Thus, immunity to Hsp65 has dual attributes: pathogenic as well as protective. (This figure summarizes information from multiple studies described in the text.)