CD200 receptors are differentially expressed and modulated by minocycline in the brain during Trypanosoma brucei infection.

Infection with Trypanosoma brucei, which causes African trypanosomiasis, activates microglia, which are constitutively maintained in a quiescent state through CD200-CD200 receptor interactions. C57BL/6 mice have one inhibitory receptor, CD200R and three activating members, CD200 receptor-like (RL)a-c. Infection increased MAC-1 (microglia marker), CD200RLa and CD200RLb, but not CD200, CD200R or CD200RLc, transcript levels in the brains. Minocycline treatment inhibited the infection-induced elevation of MAC-1 and CD200RLa transcripts, but had no significant effect on CD200 or the other receptors. This suggests that CD200RLa might play a role in microglia/macrophage activation during trypanosome infection.