{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T22:04:50Z","timestamp":1791065090934,"version":"4.1.0"},"reference-count":35,"publisher":"National Academy of Sciences","issue":"39","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2008,9,30]]},"abstract":"<jats:p>\n                    A recessive phenotype called\n                    <jats:italic>spin<\/jats:italic>\n                    (spontaneous inflammation) was induced by\n                    <jats:italic>N<\/jats:italic>\n                    -ethyl-\n                    <jats:italic>N<\/jats:italic>\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\n                    <jats:italic>Listeria monocytogenes<\/jats:italic>\n                    . TLR-induced TNF and IL-1 production are normal in macrophages derived from\n                    <jats:italic>spin<\/jats:italic>\n                    mice. The autoinflammatory phenotype of\n                    <jats:italic>spin<\/jats:italic>\n                    mice is fully suppressed by compound homozygosity for\n                    <jats:italic>Myd88<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>poc<\/jats:italic>\n                    <\/jats:sup>\n                    ,\n                    <jats:italic>Irak4<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>otiose<\/jats:italic>\n                    <\/jats:sup>\n                    , and\n                    <jats:italic>Il1r1<\/jats:italic>\n                    -null mutations, but not\n                    <jats:italic>Ticam1<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Lps2<\/jats:italic>\n                    <\/jats:sup>\n                    ,\n                    <jats:italic>Stat1<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>m1Btlr<\/jats:italic>\n                    <\/jats:sup>\n                    , or\n                    <jats:italic>Tnf<\/jats:italic>\n                    -null mutations. Both autoimmune and autoinflammatory phenotypes are suppressed when\n                    <jats:italic>spin<\/jats:italic>\n                    homozygotes are derived into a germ-free environment. The\n                    <jats:italic>spin<\/jats:italic>\n                    phenotype was ascribed to a viable hypomorphic allele of\n                    <jats:italic>Ptpn6<\/jats:italic>\n                    , which encodes the tyrosine phosphatase SHP1, mutated in mice with the classical\n                    <jats:italic>motheaten<\/jats:italic>\n                    alleles\n                    <jats:italic>me<\/jats:italic>\n                    and\n                    <jats:italic>me-v<\/jats:italic>\n                    . 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.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0806619105","type":"journal-article","created":{"date-parts":[[2008,9,19]],"date-time":"2008-09-19T21:33:20Z","timestamp":1221860000000},"page":"15028-15033","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":119,"title":["Inflammation and autoimmunity caused by a SHP1 mutation depend on IL-1, MyD88, and a microbial trigger"],"prefix":"10.1073","volume":"105","author":[{"given":"Ben A.","family":"Croker","sequence":"first","affiliation":[{"name":"Departments of *Genetics and"},{"name":"Cancer and Haematology Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian R.","family":"Lawson","sequence":"additional","affiliation":[{"name":"Immunology, The Scripps Research Institute, 10550 N. 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