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The Journal of Immunology, 2004, 172: 6093-6100.
Copyright © 2004 by The American Association of Immunologists

Restoration of NK T Cell Development in fyn-Mutant Mice by a TCR Reveals a Requirement for Fyn During Early NK T Cell Ontogeny 1

Paul Gadue2,3,*, Liqun Yin3,{dagger}, Sumesh Jain{ddagger} and Paul L. Stein4,{dagger}

* Graduate Group in Immunology and {dagger} Department of Dermatology, University of Pennsylvania, Philadelphia, PA 19104; and {ddagger} Department of Dermatology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611

NK T cells are a unique lymphocyte population that have developmental requirements distinct from conventional T cells. Mice lacking the tyrosine kinase Fyn have 5- to 10-fold fewer mature NK T cells. This study shows that Fyn-deficient mice have decreased numbers of NK1.1– NK T cell progenitors as well. 5-Bromo-2'-deoxyuridine-labeling studies indicate that the NK T cells remaining in fyn–/– mice exhibit a similar turnover rate as wild-type cells. The fyn–/– NK T cells respond to {alpha}-galactosylceramide, a ligand recognized by NK T cells, and produce cytokines, but have depressed proliferative capacity. Transgenic expression of the NK T cell-specific TCR {alpha}-chain V{alpha}14J{alpha}18 leads to a complete restoration of NK T cell numbers in fyn–/– mice. Together, these results suggest that Fyn may have a role before {alpha}-chain rearrangement rather than for positive selection or the peripheral upkeep of cell number. NK T cells can activate other lymphoid lineages via cytokine secretion. These secondary responses are impaired in Fyn-deficient mice, but occur normally in fyn mutants expressing the V{alpha}14J{alpha}18 transgene. Because this transgene restores NK T cell numbers, the lack of secondary lymphocyte activation in the fyn-mutant mice is due to the decreased numbers of NK T cells present in the mutant, rather than an intrinsic defect in the ability of the other fyn–/– lymphoid populations to respond.




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