This is in keeping with the ranibizumab studies. However, an increase in macular thickness of at least 20% was observed in 50% of these participants by 24 months. This observation AbMole 3,4,5-Trimethoxyphenylacetic acid mirrors the CATT study, in which persistent fluid at the macula was more frequently observed in the bevacizumab arm compared to Ranibizumab. This delayed non-response or rebound phenomenon also merit further evaluation in future studies. The inherent limitation of this study is the small sample size. Nevertheless, the trends shown in these exploratory analyses justify further investigation, since they have important implications on the potential choice of anti-VEGF agent to use in eyes with DMO. Another limitation is the use of Stratus OCT, a time domain OCT which is subject to frequent artefacts and lower repeatability compared to spectral-domain OCT. Further sufficiently powered clinical trials comparing various antiVEGF agents with at least 24 months follow-up and using spectral domain OCT will better inform clinicians on subtle differences in the effects on macular thickness profiles. Following recognition of an antigen on the surface of a major histocompatibility complex molecule, the T cell receptor initiates a number of signaling cascades that determine cytokine production, cell survival, proliferation and differentiation. The initial event, phosphorylation of immunoreceptor tyrosine-based activation motifs on the cytosolic side of the TCR/CD3�� chain complex, allows for Zap70 to be recruited to CD3��. Zap70 becomes activated in this way and promotes the recruitment and phosphorylation of other adaptor molecules responsible of transmitting signals downstream. Several studies have shown that TCR signaling is modified in patients suffering from SLE. Instead of transmitting signals through TCR to CD3�� and Zap70, an alternative pathway comes into play involving FcR�� and spleen tyrosine kinase. FcR�� is homologous in shape and function to CD3�� and takes its place in SLE T cells and associates with Syk. This alternative FcR��/Syk duet is 100 times enzymatically more potent than the canonical CD3��/Zap70. As a result, following activation, SLE T cells exhibit higher intracytoplasmic calcium flux and cytosolic protein tyrosine phosphorylation. To better understand the contribution of Syk in the aberrant phenotype of SLE T cells we examined the effect of Syk on the expression of molecules known to contribute to the pathogenesis of SLE. A two-step approach was followed: Syk was overexpressed in healthy blood-donor T cells to examine whether increased Syk expression creates SLE-like phenotype; and Syk was downregulated, using siRNA, in SLE T cells to examine whether gene expression abnormalities can be corrected. Our results show that Syk contributes significantly to the abnormal expression of a number of molecules associated with the immunopathogenesis of SLE.