The surrounding cells provide a sheltering environment that shields SCs from stimuli that may adversely promote differentiation and apoptosis and threaten the SC reservoir. Notably, the limbus is highly pigmented, due to the presence of melanocytes that have been infiltrated by antigen-presenting Langerhan��s cells and suppressor T-lymphocytes, and is surrounded by a vascular network. Melanocytes may produce and transport melanin pigments into epithelial cells to minimize damage caused by ultraviolet irradiation, similar to an effect described in the SCcontaining bulge area of human skin. The BM of the limbal epithelium differs from that of the central cornea. For example, the percentage of basal cell membrane occupied by hemidesmosomes was found to be significantly less than that of the central cornea. Unlike that of the cornea, the BM of the limbus is undulating, with papillae or pegs of stroma extending upward and fenestrated by so-called limbal crypts and focal stromal projections; the central cornea lacks such papillae. The anatomic features present in the limbus suggest that limbal SCs might closely interact with cells in the underlying limbal stroma. The unique BM structures of the limbal area are constructed as a Picroside-I result of the preferential expression of a9 integrin and N-cadherin without connexin 43, suggesting that limbal SCs are 4-(Aminomethyl)benzoic acid influenced by the interaction with the unique extracellular components in the niche. Aside from laminin-1 and laminin-5, the limbal BM also contains laminin a2b2 chains, while the corneal BM does not. Moreover, a1, a2, and a5 chains of type IV collagen are present in the limbal BM, while a3 and a5 chains are present in its corneal counterpart. All of these components might contribute to the distribution of SC in this niche, as has been suggested for intestinal crypt villi. Furthermore, like other SC niches the limbal BM might sequester and, hence, modulate concentrations of growth factors and cytokines that are released from limbal cells in the niche for efficient and precise targeting onto limbal SCs. These observations suggest that the corneal epithelial BM may affect the overlying epithelial phenotype. In animal studies, LSCT over the limbal area for treating limbal deficiency has shown that limbal SCs are able to provide new healthy corneal epithelial cells and restore the lost niches of the stromal layer, thus compensating for the regression of vessels and the rearrangement of stromal lamellae due to limbal SC deficiency.