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The Journal of Immunology, 1999, 163: 2681-2687.
Copyright © 1999 by The American Association of Immunologists

T Cell Development in PU.1-Deficient Mice1

Lisa M. Spain2,*, Anastasia Guerriero{dagger}, Sudeesha Kunjibettu* and Edward W. Scott2,{dagger}

* Wistar Institute, Philadelphia, PA 19104; and {dagger} Institute for Human Gene Therapy, University of Pennsylvania Medical School, Philadelphia, PA 19104.

These studies address the role of PU.1 in T cell development through the analysis of PU.1-/- mice. We show that the majority of PU.1-/- thymocytes are blocked in differentiation prior to T cell commitment, and contain a population of thymocyte progenitors with the cell surface phenotype of CD44+, HSAbright, c-kitint, Thy-1-, CD25-, Sca-1-, CD4-, and CD8-. These cells correspond in both number and cell surface phenotype with uncommitted thymocyte progenitors found in wild-type fetal thymus. RT-PCR analysis demonstrated that PU.1 is normally expressed in this early progenitor population, but is down-regulated during T cell commitment. Rare PU.1-/- thymi, however, contained small numbers of thymocytes expressing markers of T cell commitment. Furthermore, almost 40% of PU.1-/- thymi placed in fetal thymic organ culture are capable of T cell development. Mature PU.1-/- thymocytes generated during organ culture proliferated and produced IL-2 in response to stimulation through the TCR. These data demonstrate that PU.1 is not absolutely required for T cell development, but does play a role in efficient commitment and/or early differentiation of most T progenitors.




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