Taken together, the above findings suggest that an efficient and safe cell-selection system combining AQP expression and ultra-quick freezing could be used as a novel method for selecting or concentrating cells for diverse purposes from basic to clinical applications. In viral infections, however, CD8+ cytotoxic T lymphocyte function is central to immune response, mediating effective clearance of infected and transformed cells; virusspecific CD8+ T cells also play a role in immune surveillance in HTLV-1 leukemogenesis. CTL dysfunction, however, results in viral persistence. Constant antigenic stimulation due to chronic hyper-antigenemia in the context of viral persistence induces T-cell exhaustion, a state characterized by impaired CTL function. This can be attributed in part to the presence of co-inhibitory markers involved in modulating T-cell response to infection. In mouse models of chronic viral infection with lymphocytic choriomeningitic virus infection, CTLs demonstrated increased expression of co-inhibitory receptors and reduced cytolytic function as has been reported for Hepatitis B virus, Hepatitis C virus and Human immunodeficiency virus infections in humans. CTL function in the different viral infections. 2B4/CD244, a member of the signaling lymphocyte activation molecule ARRY-142886 supply family of CD2 related receptors is upregulated in chronic viral infections. 2B4 is the only SLAM family receptor known to have variable interactions with its known ligand CD48. 2B4 is expressed on natural killer cells, CD8+ T cells, basophils, monocytes and eosinophils. The ligand, CD48, is a glycophosphatidyl anchored receptor with high affinity for 2B4 expressed on both lymphoid and myeloid cells and known to be involved in modulation of CTL function. CD48 is upregulated on B-cells in Epstein-Barr virus infection and down regulated in HIV infected cells. Ligation of the 2B4 receptor by CD48 has been shown to be involved in the development of lytic activity on T cells, however, it is not always clear whether ligation results in inhibitory or stimulatory effect on CTL activity due to conflicting findings from existing studies and the discovery of SAP, a post receptor intracellular adapter expressed on natural killer cells, T-cells and involved in signal transduction of SLAM family members, including 2B4 and CD48. 2B4-CD48 interaction has been variably shown to either activate or inhibit effector function; this however depends on levels of SAP expression; in the presence of insufficient SAP or its absence, inhibitory and stimulatory if high. Increased 2B4 receptor expression or CD48 ligand density could also render SAP limiting. The interaction of these receptors with their ligands results in reduced T cell function and blockade of this interaction improved CTL function in the different viral infections. Existing studies tend to focus on 2B4 expression on NK cells with less emphasis on the role of 2B4 on CTL function.