Imperial College London
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DrSophieRutschmann

Faculty of Medicine, Department of Immunology and Inflammation

Reader in Immunology
 
 
 
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Contact

 

s.rutschmann Website

 
 
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Location

 

9N4bHammersmith HospitalHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Croker:2008:10.1073/pnas.0806619105,
author = {Croker, BA and Lawson, BR and Rutschmann, S and Berger, M and Eidenschenk, C and Blasius, AL and Moresco, EMY and Sovath, S and Cengia, L and Shultz, LD and Theofilopoulos, AN and Pettersson, S and Beutler, BA},
doi = {10.1073/pnas.0806619105},
journal = {Proc Natl Acad Sci U S A},
pages = {15028--15033},
title = {Inflammation and autoimmunity caused by a SHP1 mutation depend on IL-1, MyD88, and a microbial trigger.},
url = {http://dx.doi.org/10.1073/pnas.0806619105},
volume = {105},
year = {2008}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - A recessive phenotype called spin (spontaneous inflammation) was induced by N-ethyl-N-nitrosourea (ENU) mutagenesis in C57BL/6J mice. Homozygotes display chronic inflammatory lesions affecting the feet, salivary glands and lungs, and antichromatin antibodies. They are immunocompetent and show enhanced resistance to infection by Listeria monocytogenes. TLR-induced TNF and IL-1 production are normal in macrophages derived from spin mice. The autoinflammatory phenotype of spin mice is fully suppressed by compound homozygosity for Myd88(poc), Irak4(otiose), and Il1r1-null mutations, but not Ticam1(Lps2), Stat1(m1Btlr), or Tnf-null mutations. Both autoimmune and autoinflammatory phenotypes are suppressed when spin homozygotes are derived into a germ-free environment. The spin phenotype was ascribed to a viable hypomorphic allele of Ptpn6, which encodes the tyrosine phosphatase SHP1, mutated in mice with the classical motheaten alleles me and me-v. Inflammation and autoimmunity caused by SHP1 deficiency are thus conditional. The SHP1-deficient phenotype is driven by microbes, which activate TLR signaling pathways to elicit IL-1 production. IL-1 signaling via MyD88 elicits inflammatory disease.
AU  - Croker,BA
AU  - Lawson,BR
AU  - Rutschmann,S
AU  - Berger,M
AU  - Eidenschenk,C
AU  - Blasius,AL
AU  - Moresco,EMY
AU  - Sovath,S
AU  - Cengia,L
AU  - Shultz,LD
AU  - Theofilopoulos,AN
AU  - Pettersson,S
AU  - Beutler,BA
DO  - 10.1073/pnas.0806619105
EP  - 15033
PY  - 2008///
SP  - 15028
TI  - Inflammation and autoimmunity caused by a SHP1 mutation depend on IL-1, MyD88, and a microbial trigger.
T2  - Proc Natl Acad Sci U S A
UR  - http://dx.doi.org/10.1073/pnas.0806619105
UR  - https://www.ncbi.nlm.nih.gov/pubmed/18806225
VL  - 105
ER  -
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