To report the outcomes of infliximab therapy in the treatment of ocular inflammatory disease refractory to traditional immunomodulatory therapy (IMT). Methods:We retrospectively reviewed the medical records of 27 patients. All patients had noninfectious ocular inflammatory disease refractory to traditional IMT and received 5 mg/kg of infliximab at 2-week to 8-week intervals. Main outcome measures were clinical response, reduction in concomitant IMT, and adverse effects. Cumulative incidences of inflammation control and vision change were calculated using life-table methods.Results: Twenty-one patients experienced sustained improvement in inflammation with their initial course of infliximab therapy. Cumulative incidence of inflammation resolution at 12 months was greater than 90%. Sixteen patients were able to decrease the dose of their concomitant IMT medication or stop all other IMT. Four patients were able to discontinue all other IMT while receiving infliximab therapy. Three patients with scleritis were eventually able to remain inflammation-free while not taking any medication. At 12 months, 56% and 65% of left and right eyes, respectively, showed visual acuity improvement by 2 or more Snellen lines. Only 1 patient developed an adverse event requiring therapy discontinuation. Conclusions:We found a high rate of ocular inflammation control with infliximab therapy. The incidence of adverse effects in this study was low.
The shunt arrangement, which connects the anterior chamber to potentially microbe-populated cavities or to the lower lid fornix and its flora, might be suspected to allow rapid retrograde invasion of infective agents, resulting in endophthalmitis. In this series of KPro patients, however, the incidence of severe infection was very low, in fact comparable to that after standard trabeculectomy.
We describe the use of a soluble CD81-Fc fusion protein to screen for novel monoclonal antibody (MAb) reactive with the extracellular loops of murine CD81 (TAPA-1). Two such MAbs, Eat1 and Eat2 (for Extracellular Anti-TAPA1), were used to assess the expression and function of CD81 on murine lymphocytes. Although CD81 is expressed uniformly on all human lymphocytes, murine CD81 was found to be expressed at much higher levels on resting B cells than on resting T cells. This was particularly evident when staining with the new MAbs, Eat1 and Eat2. The molecule is also functionally active on B cells, as Eat1 and Eat2 induce homotypic adhesion of B lymphocytes. Stimulated B cells undergo early apoptotic events in the presence of Eat2, as shown by binding of Annexin V-fluorescein isothiocyanate (FITC). Polyclonal activation of murine T cells also induces higher level CD81 expression, and many immortalized murine T-cell lines express high levels of the protein. In contrast to human CD81, which is expressed equally on all thymocytes, murine CD81 is induced during thymic development, being expressed at high levels on CD4+CD8+ thymocytes, in contrast to other subsets of thymocytes. Finally, murine dendritic cells, splenic macrophages, and non-killer (NK) cells all express high levels of CD81. We conclude that CD81 is differentially expressed in the murine immune system, and is involved in regulating the adhesion and activation of murine B cells.
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