Abstract:
:Tristetraprolin (TTP) is a widely expressed potential transcription factor that contains two unusual CCCH zinc fingers and is encoded by the immediate-early response gene, Zfp-36. Mice made deficient in TTP by gene targeting appeared normal at birth, but soon manifested marked medullary and extramedullary myeloid hyperplasia associated with cachexia, erosive arthritis, dermatitis, conjunctivitis, glomerular mesangial thickening, and high titers of anti-DNA and antinuclear antibodies. Myeloid progenitors from these mice showed no increase in sensitivity to growth factors. Treatment of young TTP-deficient mice with antibodies to tumor necrosis factor alpha (TNF alpha) prevented the development of essentially all aspects of the phenotype. These results indicate a role for TTP in regulating TNF alpha synthesis, secretion, turnover, or action. TTP-deficient mice may serve as useful models of the autoimmune inflammatory state resulting from chronic effective TNF alpha excess.
journal_name
Immunityjournal_title
Immunityauthors
Taylor GA,Carballo E,Lee DM,Lai WS,Thompson MJ,Patel DD,Schenkman DI,Gilkeson GS,Broxmeyer HE,Haynes BF,Blackshear PJdoi
10.1016/s1074-7613(00)80411-2subject
Has Abstractpub_date
1996-05-01 00:00:00pages
445-54issue
5eissn
1074-7613issn
1097-4180pii
S1074-7613(00)80411-2journal_volume
4pub_type
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