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Interferons α / β inhibit IL‐7‐induced proliferation of CD4 − CD8 − CD3 − CD44 + CD25 + thymocytes, but do not inhibit that of CD4 − CD8 − CD3 − CD44 − CD25 − thymocytes
Author(s) -
SU D.M.,
WANG J.,
LIN Q.,
COOPER M. D.,
WATANABE T.
Publication year - 1997
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1997.00205.x
Subject(s) - il 2 receptor , cd8 , biology , microbiology and biotechnology , cd44 , cd3 , thymocyte , population , t lymphocyte , t cell , endocrinology , medicine , immunology , immune system , biochemistry , cell , environmental health
Type 1 interferons (IFN‐ α/β ) have recently been shown to inhibit interleukin‐7 (IL‐7)‐induced growth and survival of early B‐lineage cells. The CD3 − CD4 − CD8 − (triple negative; TN) thymocytes from normal mice strongly proliferated upon stimulation with IL‐7 in suspension culture. Such an IL‐7‐induced proliferation was suppressed by the addition of IFN‐ α/β , but a fraction of the TN thymocytes still showed proliferation. The IL‐7‐induced growth of TN thymocytes from scid mice, which lack the CD44 − CD25 − subpopulation, was completely inhibited by the addition of IFN‐ α/β . The IL‐7 induced proliferation of CD4 − CD8 − thymocytes from T‐cell receptor (TCR) transgenic mice, the majority of which are CD3 + CD44 − CD25 − , was resistant to IFN‐ α/β ‐mediated suppression. In fetal thymus organ cultures (FTOC), the addition of IL‐7 greatly increased the population of CD4 − CD8 − CD44 + CD25 + thymocytes and IFN‐ α/β inhibited this IL‐7‐driven expansion. In contrast, the addition of IL‐7 markedly decreased the percentages of CD4 − CD8 − CD3 − CD44 − CD25 − cells, and IFN‐ α/β reversed the effect and increased the subpopulations of CD44 − CD25 + and CD44 − CD25. − Finally, IFN‐ β mRNA was found to be expressed in the thymus. The data suggest that type 1 interferons inhibit IL‐7‐driven proliferation of TN thymocytes, but do not block the normal differentiation process.