Traffic of Hematogenous Cells Through the Central Nervous System

Williams, Kenneth C.; Hickey, William F.

doi:10.1007/978-3-642-79657-9_15

Cited by 62 publications

(59 citation statements)

References 128 publications

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“…Myelin oligodendrocyte glycoprotein (MOG) 35-55 is a well-characterized target Ag of encephalitogenic T cells used to initiate EAE in the H-2 b C57B/6 mouse model (5). Studies have shown that T cell trafficking to the CNS is a critical factor in the ability of CD4 ϩ T cells to mediate disease (6). Adhesion molecules facilitate the infiltration of lymphocytes into the CNS of mice with EAE.…”

mentioning

confidence: 99%

CD43 Modulates Severity and Onset of Experimental Autoimmune Encephalomyelitis

Ford

Onami

Sperling

et al. 2003

The Journal of Immunology

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Experimental autoimmune encephalomyelitis (EAE) is a mouse model of multiple sclerosis characterized by infiltration of activated CD4+ T lymphocytes into tissues of the CNS. This study investigated the role of CD43 in the induction and progression of EAE. Results demonstrate that CD43-deficient mice have reduced and delayed clinical and histological disease severity relative to CD43+/+ mice. This reduction was characterized by decreased CD4+ T cell infiltration of the CNS of CD43−/− mice but similar numbers of Ag-specific T cells in the periphery, suggesting a defect in T cell trafficking to the CNS. The absence of CD43 also affected cytokine production, as myelin oligodendrocyte glycoprotein (MOG) 35–55-specific CD43−/− CD4+ T cells exhibited reduced IFN-γ and increased IL-4 production. CD43−/− CD4+ MOG-primed T cells exhibited reduced encephalitogenicity relative to CD43+/+ cells upon adoptive transfer into naive recipients. These results suggest a role for CD43 in the differentiation and migration of MOG35–55-specific T cells in EAE, and identify it as a potential target for therapeutic intervention.

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mentioning

confidence: 99%

CD43 Modulates Severity and Onset of Experimental Autoimmune Encephalomyelitis

Ford

Onami

Sperling

et al. 2003

The Journal of Immunology

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“…However, T cells that recognize Ags present in the CNS are preferentially retained (16). After splenocytes were transferred from B6 mice to MHV-infected RAG 1 Ϫ/Ϫ mice, a large fraction of CD4 and CD8 T cells present in the CNS recognized MHV-specific epitopes (20 -22).…”

mentioning

confidence: 99%

Bystander CD8 T Cell-Mediated Demyelination After Viral Infection of the Central Nervous System

Haring¹,

Pewe

Perlman

2002

The Journal of Immunology

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Multiple sclerosis, a chronic inflammatory disease of the CNS, is characterized by immune-mediated demyelination. Many patients have a remitting-relapsing course of disease with exacerbations often following unrelated microbial illnesses. The relationship between the two events remains obscure. One possibility is that T cells specific for the inciting microbial pathogen are able to effect demyelination at a site of ongoing inflammation within the CNS. This possibility was examined in mice infected with mouse hepatitis virus, a well-described model of virus-induced demyelination. Using transgenic TCR/recombination activation gene 2−/− mice with only non-mouse hepatitis virus-specific T cells, we show that CD8 T cells are able to cause demyelination in the absence of cognate Ag in the CNS, but only if specifically activated. These findings demonstrate a novel mechanism for immune-mediated neuropathology and show that activated CD8 T cells may serve as important mediators of bystander demyelination during times of infection, including in patients with multiple sclerosis.

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“…In 1982, Bill Narayan postulated the "Trojan Horse" hypothesis whereby visna virus (one of the first lentiviruses described in detail) entered brains of sheep and goats by hiding within circulating monocytes and then once in the brain, emerged to cause disease (Narayan et al, 1982). It has been proposed that circulating monocytes enter the brain during normal immune surveillance (Williams and Hickey, 1995). However, this remains an issue of debate (Fischer-Smith and Rappaport, 2005).…”

Section: Lentiviral Encephalitismentioning

confidence: 99%

“…CCL2 mRNA was upregulated in cultured astrocytes, but remained at low levels compared to CCL7, suggesting a role for CCL7 in HIV-related encephalitis . Even under noninflamed conditions CCL7 is expressed in the brain , Sasseville et al, 1996, which could contribute to basal levels of monocyte migration into the brain for "routine surveillance" (Williams and Hickey, 1995). That CCL7 is upregulated by astrocytes in response to cytokines present in encephalitic brains gives a potential role for controlling monocyte migration during encephalitis as well (Sasseville et al, 1996.…”

Section: Expression and Secretion Of Selected Chemokinesmentioning

confidence: 99%