Abstract:
:SOCS1-/- mice die prematurely of increased interferon-gamma (IFNgamma) signaling with severe thymic atrophy and accelerated maturation of T cells. However, it was unclear whether the thymic defects were caused by SOCS1 deficiency or by increased IFNgamma signaling. Using SOCS1-/- IFNgamma-/- mice, we show in this study that SOCS1 deficiency skews thymocyte development toward CD8 lineage independently of IFNgamma. Fetal thymic organ cultures and intrathymic transfer of CD4-CD8- precursors into Rag1-/- mice show that the lineage skewing in SOCS1-/- mice is a T-cell autonomous defect. Interestingly, SOCS1 is not required for attenuating interleukin-7 (IL-7) signaling at the CD4-CD8- stage but is essential for regulating IL-15 and IL-2 signaling in CD8+ thymocytes. IL-15 selectively stimulates SOCS1-/- CD8+ thymocytes, inducing sustained signal transducer and activator of transcription 5 (STAT5) phosphorylation and massive proliferation. IL-15 also strongly up-regulates Bcl-xL and CD44 in CD8+ thymocytes lacking SOCS1. The SOCS1 gene is induced in CD4+ thymocytes by gammac cytokines, whereas CD8+ thymocytes constitutively express SOCS1 mRNA even in the absence of cytokine stimulation. Because many different cell types express IL-15, our results strongly suggest that SOCS1 functions as an indispensable attenuator of IL-15 receptor signaling in developing CD8+ thymocytes.
journal_name
Bloodjournal_title
Bloodauthors
Ilangumaran S,Ramanathan S,Ning T,La Rose J,Reinhart B,Poussier P,Rottapel Rdoi
10.1182/blood-2003-01-0175subject
Has Abstractpub_date
2003-12-01 00:00:00pages
4115-22issue
12eissn
0006-4971issn
1528-0020pii
2003-01-0175journal_volume
102pub_type
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