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SOCS1 deficiency causes a lymphocyte-dependent perinatal lethality.

SOCS1 is an SH2-containing protein that is primarily expressed in thymocytes in a cytokine- and T cell receptor-independent manner. SOCS1 deletion causes perinatal lethality with death by 2-3 weeks. During this period thymic changes include a loss of cellularity and a switch from predominantly CD4+ CD8+ to single positive cells. Peripheral T cells express activation antigens and proliferate to IL-2 in the absence of anti-CD3. In addition, IFNgamma is present in the serum. Reconstitution of the lymphoid lineage of JAK3-deficient mice with SOCS1-deficient stem cells recapitulates the lethality and T cell alterations. Introducing a RAG2 or IFNgamma deficiency eliminates lethality. The results demonstrate that lymphocytes are critical to SOCS1-associated perinatal lethality and implicate SOCS1 in lymphocyte differentiation or regulation.

Pubmed ID: 10490100


  • Marine JC
  • Topham DJ
  • McKay C
  • Wang D
  • Parganas E
  • Stravopodis D
  • Yoshimura A
  • Ihle JN



Publication Data

September 3, 1999

Associated Grants

  • Agency: NCI NIH HHS, Id: CA21765
  • Agency: NHLBI NIH HHS, Id: P01 HL53749
  • Agency: NIDDK NIH HHS, Id: R01 DK42932

Mesh Terms

  • Age Factors
  • Animals
  • Animals, Newborn
  • Carrier Proteins
  • DNA-Binding Proteins
  • Dose-Response Relationship, Drug
  • Flow Cytometry
  • Gene Expression Regulation, Developmental
  • Interferon-gamma
  • Janus Kinase 3
  • Lymphocytes
  • Mice
  • Mice, Mutant Strains
  • Protein-Tyrosine Kinases
  • Repressor Proteins
  • Suppressor of Cytokine Signaling Proteins
  • T-Lymphocytes
  • Thymus Gland
  • Tissue Distribution