Chi-Chao Chan

　　Background：Age-related macular degeneration(AMD)is a leading course of blindness worldwide among the elderly.The etiology of AMD remains unclear.While it is not a classical inflammatory disease like uveitis，inflammatory cells，especially macrophages，have long been recognized as key players in AMD pathogenesis。

　　Method:Using routine histology，immunohistochemistry and RQ-PCR we determined macrophage subtypes in choroidal buttons in the macular region of 15 AMD cases and 25 controls，plus a choroidal neovascular membrane that was resistant to multiple avastin treatment。

　　Results:With aging，the macular choroids showed increasing sclerosis and decreased macrophages，especially M2-macrophages，but higher M2 cytokine(CCL22)transcripts.Compared with the age-matched non-AMDs，the AMD choroids showed more sclerosis，less M2-macrophages，lower M2(CCL22)transcript，and higher ratio of M1/M2(CXCL11/CCL22)chemokines.The CNVM was infiltrated with predominantly M1 macrophages with high CXCL11 expression and Th17 lymphocytes with high IL-17 expression。

　　Conclusion:Normal aging is associated with decreased macrophage infiltration，but increased activity of M2-macrophage.AMD eyes exhibit significant decreases of M2-macrophage activities and a shift in macrophage activity towards M1-macrophages.The CNVM of the bevacizumab-resist AMD patient showed active M1-macrophage and Th17 lymphocyte.M1-macrophage could play an important role in AMD pathogenesis，promoting inflammation and accelerating CNV formation.Anti-inflammatory agents may be considered for those AMD patients who fail anti-VEGF therapy.