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B Cell Induction of IL-13 Expression in NK Cells: Role of CD244 and SLAM-Associated Protein

Ning Gao^*, Pamela Schwartzberg, Julie A. Wilder, Bruce R. Blazar and Dorothy Yuan^1,*

^* Department of Molecular Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390; National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892; Lovelace Respiratory Research Institute, Albuquerque, NM 87108; and Department of Pediatrics, Division of Blood and Marrow Transplantation, and Cancer Center, University of Minnesota Hospital and Cancer Center, Minneapolis, MN 55455

NK cells are an important component of the innate immune system that can also interact with B cells in a mutually productive manner. We have previously shown that activated B cells can induce NK cells to up-regulate their secretion of IFN-. In this study, we show that B cells, and, particularly, marginal zone B cells, can, in addition, induce NK cells via direct cell-cell interactions to express mRNA encoding the Th2 cytokine IL-13. The induction of NK cell IL-13 mRNA expression requires the ligation of the CD244 receptor by the CD48 ligand on B cells via signaling pathways that depend upon expression of the X-linked lymphoproliferative disease gene product, SH2D1A/DSHP/SAP (SLAM-associated protein, or SAP) in NK cells. Thus, the positive signals attributed to the B cell activation of CD244 on murine NK cells appears to be more similar to the activity of CD244 on human cells. The induction of IL-13 mRNA by B cells may account for the effect of NK cells on the generation of Th2-type responses in the presence of some adjuvants.

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