SOCS1 deficiency causes a lymphocyte-dependent perinatal lethality. Cell 1999 Sep 03;98(5):609-16
Date
09/18/1999Pubmed ID
10490100DOI
10.1016/s0092-8674(00)80048-3Scopus ID
2-s2.0-0033520467 (requires institutional sign-in at Scopus site) 468 CitationsAbstract
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.
Author List
Marine JC, Topham DJ, McKay C, Wang D, Parganas E, Stravopodis D, Yoshimura A, Ihle JNAuthor
Demin Wang PhD Professor in the Microbiology and Immunology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Age FactorsAnimals
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 1 Protein
Suppressor of Cytokine Signaling Proteins
T-Lymphocytes
Thymus Gland
Tissue Distribution
