Abstract

Editor:
I read the recent publication on the role of the class II major histocompatibility complex (MHCII) in leptospirosis by Radaelli et al 3 with great interest. Radaelli et al concluded that “results suggest that during leptospiral nephritis, MHCII contributes to the intensity of the inflammatory response. Furthermore de novo MHCII expression in regenerating tubules may play a role in the defense mechanism against leptospiral tubular colonization.” Indeed, the role of MHC in leptospirosis is still a mystery. Barbosa et al 1 recently reported that binding of C4BP contributed to leptospiral serum resistance against host complement in human beings. For the horse, Kalsow et al 2 found that leptospiral-induced retinal pathology might be a primary immunological event, relating to MHCII, in equine uveitis. The exact clinical correlation between MHCII expression and host pathology needs further studies.
