Author/Authors :
Yin-Ji Li، نويسنده , , Zhihong Xu and Kang Chong ، نويسنده , , Mi-Ran and Choi، نويسنده , , Jong-Sung and Jeon، نويسنده , , Hak-Soo and Han، نويسنده , , Heon-Seok and Kim، نويسنده , , Ji-Yoon and Son، نويسنده , , Bo-Ra and Lee، نويسنده , , Young-Min and Hahn، نويسنده , , Youn-Soo، نويسنده ,
Abstract :
Immune reactivity to autologous heat shock protein 60 (HSP60) has been reported to be associated with a favorable prognosis in autoimmune diseases. To provide a clue for the possible role of HSP60 in Kawasaki disease (KD), we investigated the levels of intra- and extracellular HSP60 in the course of KD. In KD patients, autologous HSP60 was abundantly expressed in CD11c+ cells during the acute phase and subsequently decreased during the subacute phase. Most of HSP60-expressing CD11c+ cells observed in the acute phase was composed of CD11clow cells instead of CD11chigh cells, which were dominant in the subacute phase. In contrast, circulating HSP60 levels were higher in the subacute phase than those in the acute phase, reflecting higher level of HSP60 exposure to the immune system of patients during recovery. These changes in the levels of intra- and extracellular HSP60 were not observed in patients with other febrile diseases. The observed features of HSP60 expression in patients with KD are in favor of a role for autologous HSP60 as a regulator for control of inflammation, rather than a proinflammatory mediator in KD.