Primary Open Angle Glaucoma (POAG) is a blindness causing disease. The main risk factor for POAG is elevated intraocular pressure (IOP) due to insufficient outflow of aqueous humor from the eye into the vasculature. Carbohydrate- based recognition systems are increasingly recognized for their roles in physiological as well as pathogenic processes. These systems are comprised of a glycan message carried by a glycoprotein or glycolipid and a message decoder, a carbohydrate binding protein (lectin). The trabecular meshwork (TM), a prominent participant in the regulation of aqueous humor outflow facility shows expression of various lectins, including members of the classic families I-type lectins, C-type lectins and S-type lectins (Galectins). Some of these lectins, namely ICAM-1, E- and P-selectins have altered expression levels in TM derived from eyes with POAG. Another, CD44 shows elevated levels in the POAG aqueous humor. Many carbohydrate recognizing proteins, upon binding to their respective countereceptors can affect cellular processes shown to be paramount for the maintenance of outflow facility by TM. This review will survey lectins known to be expressed in TM, their known and hypothesized functions in the tissue and highlight some interesting venues for study of putative roles for lectins in the disease-promoting mechanisms taking place in POAG TM.