Using a mouse model of MS, Klenmann et al found that AM80, a synthetic molecule related to vitamin A, inhibited Th17 T cell function without generating general immunosuppression. AM80 treatment was effective in inhibiting early symptoms in the MS mouse model, even if administered after disease initiation, but it did not prevent chronic symptoms.
Drs. Yamamura, Oki, and colleagues "conclude that treatment with the synthetic retinoid AM80 is a considerable intervention strategy for the acute phase of Th17-mediated autoimmune diseases such as MS."
Klemann C, Raveney BJE, Klemann AK, Ozawa T, von Hrsten S, Shudo K, Oki S, Yamamura T: Synthetic retinoid AM80 inhibits Th17 cells and ameliorates EAE. Am J Pathol 2009, 174: 2234-2245
Repair After Eye Injury
Drs. Sandrine Joly, Charlotte Rem, and colleagues have discovered that both resident and circulating cells remove damaged cells after eye injury. These results are presented in the June 2009 issue of the American Journal of Pathology.
The eyes, like the brain, are an immune-privileged site; the so called blood-retinal barrier limits access of immune cells to the eyes. After eye damage, however, immune cells remove damaged cells.
To locate the source of the immune cells that respond to retinal injury, Joly et al used a mouse model of light-induced photodamage. They found that both resident and circulating (from the bone marrow) immune cells were involved in removal of dead retinal cells. The circulating cells entered the eye without damaging the blood-retinal barrier, and both circulating and resident immune cells entered the blood stream after removing the dead cells.
Joly et al suggest that this process may "enable an immunization against retinal proteins. Specific retinal pr
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American Journal of Pathology