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Publication : Peripheral Thy1+ lymphocytes rearranging TCR-gammadelta genes in LAT-deficient mice.

First Author  Miazek A Year  2009
Journal  Eur J Immunol Volume  39
Issue  9 Pages  2596-605
PubMed ID  19701892 Mgi Jnum  J:152149
Mgi Id  MGI:4356357 Doi  10.1002/eji.200939252
Citation  Miazek A, et al. (2009) Peripheral Thy1+ lymphocytes rearranging TCR-gammadelta genes in LAT-deficient mice. Eur J Immunol 39(9):2596-605
abstractText  Linker for activation of T cells (LAT) is an adaptor molecule indispensable for development of alphabeta and gammadelta T lymphocytes. Surprisingly, using a new model of LAT-deficient mice we found that despite arrested thymic development, a discrete population of cells with active Lat promoter, expressing Thy1 molecules, accumulated in peripheral lymphoid organs of homozygous (Lat(Inv/Inv)) mutant mice. By measuring frequencies of TCR gene rearrangements in conjunction with a panel of cell surface Ag, we dissected two subsets of these Thy1(+) cells. Thy1(dull) cells expressed markers of NK lymphocytes and contained low frequency of TCR-gamma gene rearrangements without detectable TCR-delta rearrangements. Thy1(high) cells resembled immature CD44(+)CD25(+) thymocytes and contained high frequency of non-productive TCR-gamma and TCR-delta rearrangements, indicating that cells displaying molecular signatures of commitment toward gammadelta T-cell lineage can develop and populate lymphoid tissues of LAT-deficient mice. Phenotypically similar Thy1(high) cells were also found in lymph nodes of lymphocyte-deficient (Rag2(-/-)) mice but not in T lymphocyte proficient, heterozygous Lat(+/Inv) mice suggesting that Thy1(high) cells of LAT-deficient mice identified in this study accumulate in peripheral lymphoid organs as a result of congenital lymphopenia.
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