Abstract
NK cells are able to form a functional memory suggesting that some NK cells are surviving the activation process. We hypothesized that NK cell activation causes the development of a distinct NK cell subset and studied the fate of murine post-activation NK cells. Activation was achieved by in vivo and in vitro exposures to the melanoma tumor cell line B16 that was followed by differentiation in IL-2. When compared with control NK cells, post-activation CD25+ NK cells expressed little granzyme B or perforin and had low lysis activity. Post-activation NK cells expressed CD27, CD90, CD127, and were low for CD11b suggesting that tumor-induced activation is restricted to an early NK cell subset. Activation of NK cells led to decreases of CD16, CD11c and increases of CD62L and the IL-18 receptor. In vivo activated but not control NK cells expressed a variety of cytokines that included IFNγ, TNFα, GM-CSF and IL-10. These data suggest that the exposure of a subset of peripheral NK cells to the B16 tumor environment caused an exhaustion of their cytolytic capacity but also a gain in their ability to produce cytokines.
Highlights
NK cells were identified by their capacity for spontaneous lysis of tumor cells [1]
Activation of NK cells is supported by IL-15 We were interested in studying post-activation NK cells
Activation as measured by the expression of CD25, CD69 or IFNc can be achieved by Fc receptor cross-linking, exposure to NK-sensitive tumor cells, co-incubation with mature dendritic cells, in vivo infections with bacteria such as listeria monocytogenes, among others ([1,25,26,27] and data not shown)
Summary
NK cells were identified by their capacity for spontaneous lysis of tumor cells [1]. They express unique subsets of nonpolymorphic NK cell receptors (NKRs) that deliver either activating or inhibiting signals [2]. NK cells are constantly scrutinizing somatic cells for their expression of NKR ligands. The formation of NK cell-mediated memory has been described in the murine CMV model [3]. This suggests that some NK cells must survive their initial activation to form memory cells. Our hypothesis is that post-activation NK cells would form a functional and/or phenotypical distinct NK cell subpopulation
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