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Mice genetically lacking SHP-1 (<jats:italic>me\/me<\/jats:italic>) display severe inflammatory demyelinating disease following inoculation with the Theiler's murine encephalomyelitis virus (TMEV) compared to infected wild-type mice. Therefore, it became essential to investigate the mechanisms of TMEV-induced inflammation in the CNS of SHP-1-deficient mice. Herein, we show that the expression of several genes relevant to inflammatory demyelination in the CNS of infected<jats:italic>me\/me<\/jats:italic>mice is elevated compared to that in wild-type mice. Furthermore, SHP-1 deficiency led to an abundant and exclusive increase in the infiltration of high-level-CD45-expressing (CD45<jats:sup>hi<\/jats:sup>) CD11b<jats:sup>+<\/jats:sup>Ly-6C<jats:sup>hi<\/jats:sup>macrophages into the CNS of<jats:italic>me\/me<\/jats:italic>mice, in concert with the development of paralysis. Histological analyses of spinal cords revealed the localization of these macrophages to extensive inflammatory demyelinating lesions in infected SHP-1-deficient mice. Sorted populations of CNS-infiltrating macrophages from infected<jats:italic>me\/me<\/jats:italic>mice showed increased amounts of viral RNA and an enhanced inflammatory profile compared to wild-type macrophages. Importantly, the application of clodronate liposomes effectively depleted splenic and CNS-infiltrating macrophages and significantly delayed the onset of TMEV-induced paralysis. Furthermore, macrophage depletion resulted in lower viral loads and lower levels of inflammatory gene expression and demyelination in the spinal cords of<jats:italic>me\/me<\/jats:italic>mice. Finally,<jats:italic>me\/me<\/jats:italic>macrophages were more responsive than wild-type macrophages to chemoattractive stimuli secreted by<jats:italic>me\/me<\/jats:italic>glial cells, indicating a mechanism for the increased numbers of infiltrating macrophages seen in the CNS of<jats:italic>me\/me<\/jats:italic>mice. Taken together, these findings demonstrate that infiltrating macrophages in SHP-1-deficient mice play a crucial role in promoting viral replication by providing abundant viral targets and contribute to increased proinflammatory gene expression relevant to the effector mechanisms of macrophage-mediated demyelination.<\/jats:p>","DOI":"10.1128\/jvi.01210-08","type":"journal-article","created":{"date-parts":[[2008,11,6]],"date-time":"2008-11-06T01:46:47Z","timestamp":1225936007000},"page":"522-539","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":47,"title":["Modulation of Macrophage Infiltration and Inflammatory Activity by the Phosphatase SHP-1 in Virus-Induced Demyelinating Disease"],"prefix":"10.1128","volume":"83","author":[{"given":"George P.","family":"Christophi","sequence":"first","affiliation":[{"name":"Department of Neurology"},{"name":"Department of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse, New York"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chad A.","family":"Hudson","sequence":"additional","affiliation":[{"name":"Department of Neurology"},{"name":"Department of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse, New York"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael","family":"Panos","sequence":"additional","affiliation":[{"name":"Department of Neurology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ross C.","family":"Gruber","sequence":"additional","affiliation":[{"name":"Department of Neurology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul T.","family":"Massa","sequence":"additional","affiliation":[{"name":"Department of Neurology"},{"name":"Department of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse, New York"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-3940(98)00473-X"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(02)03047-8"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/0882-4010(87)90002-7"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.23-21-07922.2003"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1002\/glia.440150407"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jcpa.2005.11.003"},{"key":"e_1_3_2_8_2","first-page":"623","volume":"9","year":"2003","unstructured":"Bennett, J. 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