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IL‐7‐Dependent Homeostatic Proliferation in the Presence of a Large Number of T Cells in Gld Mice
Author(s) -
Aranami Toshimasa,
Iclozan Cristina,
Iwabuchi Kazuya,
Onoé Kazunori
Publication year - 2004
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2004.tb03539.x
Subject(s) - interleukin 7 receptor , biology , homeostasis , t cell , cell growth , t lymphocyte , microbiology and biotechnology , adoptive cell transfer , immunology , il 2 receptor , immune system , genetics
In gld mice, CD4 and 8‐double‐negative (DN) T cells as well as naive and memory‐phenotype T cells accumulate in the peripheral lymphoid organs. Although Fas ligand (L) defect accounts for the progressive accumulation of abnormal DN T cells, the existence of other mechanisms which may be involved in the defective homeostasis in gld mice has been unclear. In this study, we analyze T‐cell homeostasis in gld mice using adoptive transfer systems. It was shown that a gld , but not C57BL/6 (B6), environment led to augmented proliferation of B6 T cells transferred without up‐regulation of CD69. Thus, the augmented T‐cell proliferation seemed to result from mal‐homeostatic proliferation even in the presence of a large number of recipient T cells. T cells from lpr mice showed no significant proliferation in the B6 environment, suggesting that the absence of Fas‐Fas L interaction was not responsible for the mal‐homeostatic proliferation. Although similar levels of IL‐7 mRNA were detected in gld and B6 spleens, the intensity of CD127 and the proportion of CD127 + cells in the T cells were significantly lower in gld mice than in B6 mice, suggesting that IL‐7 excess in a gld environment is responsible for the abnormal proliferation of transferred T cells. The administration of anti‐CD127 antibody inhibited the proliferation of transferred lymphocytes. Thus, IL‐7‐dependent proliferation seems to be involved in the abnormal proliferation of lymphocytes in gld recipients.