Cutting Edge: A NK Complex-Linked Locus Governs Acute Versus Latent Herpes Simplex Virus Infection of Neurons

Pereira, Rosemarie A.; Scalzo, Anthony A.; Simmons, Anthony

doi:10.4049/jimmunol.166.10.5869

Cited by 63 publications

(47 citation statements)

References 19 publications

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“…NKT cells (37). With characteristic rapidity of activation and abundance of cytokine secretion (19), NKT cells were attractive candidates for an investigation of Ag-dependent mechanisms in early defense against HSV.…”

Section: Discussionmentioning

confidence: 99%

Impaired Clearance of Herpes Simplex Virus Type 1 From Mice Lacking CD1d or NKT Cells Expressing the Semivariant Vα14-Jα281 TCR

Grubor‐Bauk

Simmons

Mayrhofer

et al. 2003

The Journal of Immunology

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182

141

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Ag-presenting molecule CD1 and CD1-restricted NKT cells are known to contribute to defense against a range of infectious pathogens, including some viruses. CD1-restricted NKT cells, a distinct subpopulation of T cells, have striking and rapid effector functions that contribute to host defense, including rapid production of IFN-γ and IL-4, and activation of NK cells. Consideration of the important contributions of innate and adaptive immunity to clearance of HSV prompted us to investigate the role of CD1 and of NKT cells expressing the Vα14-Jα281 TCR in the pathogenesis of HSV infection. To address this issue, we compared infection in wild-type mice with that in CD1 gene knockout (GKO) and Jα281 GKO mice. In this study, we report impaired clearance of virus and viral Ags, and more florid acute infection in mice lacking CD1 (and by inference, CD1-restricted T cells), in comparison with parental C57BL6 mice. In Jα281 GKO mice there was also impairment of virus clearance, resembling that seen in CD1 GKO mice. These results imply roles for the Vα14-Jα281 subset of NKT cells and for CD1d in control of HSV infection.

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Section: Discussionmentioning

confidence: 99%

Impaired Clearance of Herpes Simplex Virus Type 1 From Mice Lacking CD1d or NKT Cells Expressing the Semivariant Vα14-Jα281 TCR

Grubor‐Bauk

Simmons

Mayrhofer

et al. 2003

The Journal of Immunology

Self Cite

182

141

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“…NK cells are thought to contribute to stromal keratitis [28], control HSV-1 infection [29,30], and respond to a CXCL10 chemical gradient through the receptor CXCR3 [31]. However, similar numbers of NK cells were found residing in the cornea comparing HSV-1-infected WT (225 ± 70 cells/cornea pair), CXCL9−/− (260 ± 90 cells/cornea pair), and CXCL10−/− (190 ± 90/ cornea pair) mice.…”

Section: Cd4 + T Cell Infiltration Into the Cornea Is Reduced In Cxclmentioning

confidence: 99%

CD4+ T cell migration into the cornea is reduced in CXCL9 deficient but not CXCL10 deficient mice following herpes simplex virus type 1 infection

Wuest

Farber

Luster

et al. 2006

Cellular Immunology

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The role of CXCL9 and CXCL10 in the ocular immune response to herpes simplex virus type 1 (HSV-1) infection was investigated using mice deficient in either CXCL9 or CXCL10. CXCL10 but not CXCL9 deficient mice showed an increase in sensitivity to ocular virus infection as measured by an elevation in virus titer recovered in the tear film and corneal tissue. The increase in virus was associated with an increase in the expression of the chemokine CCL2 but no significant change in the infiltration of CD4 + T cells or NK cells into the corneal stroma. In contrast, a significant reduction in CD4 + T cell infiltration into the cornea was found in CXCL9 deficient mice following HSV-1 infection consistent with the absence of CXCL9 expression and reduction in expression of other chemokines including CCL3, CCL5, CXCL1, and CXCL10. Collectively, the results suggest a nonredundant role for CXCL9 and CXCL10 in response to ocular HSV-1 infection in terms of controlling virus replication and recruitment of CD4 + T cells into the cornea.

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“…1 and 2). In mice, resistance to a number of viruses, including murine CMV (MCMV), 3 herpes simplex type-1, and ectromelia viruses, genetically maps to the NK gene complex on mouse chromosome six (3)(4)(5). The Cmv1 r resistance locus for MCMV was determined to encode the NK cell activation receptor, Ly49H (6 -8).…”

Section: Dap12 Signaling Directly Augments Proproliferative Cytokine mentioning

confidence: 99%

DAP12 Signaling Directly Augments Proproliferative Cytokine Stimulation of NK Cells during Viral Infections

French

Sjölin

Kim

et al. 2006

The Journal of Immunology

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NK cells vigorously proliferate during viral infections. During the course of murine CMV infection, this response becomes dominated by the preferential proliferation of NK cells that express the activation receptor Ly49H. The factors driving such selective NK cell proliferation have not been characterized. In this study, we demonstrate that preferential NK cell proliferation is dependent on DAP12-mediated signaling following the binding of Ly49H to its virally encoded ligand, m157. Ly49H signaling through DAP12 appears to directly augment NK cell sensitivity to low concentrations of proproliferative cytokines such as IL-15. The impact of Ly49H-mediated signaling on NK cell proliferation is masked in the presence of high concentrations of proproliferative cytokines that nonselectively drive all NK cells to proliferate.

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Cutting Edge: A NK Complex-Linked Locus Governs Acute Versus Latent Herpes Simplex Virus Infection of Neurons

Cited by 63 publications

References 19 publications

Impaired Clearance of Herpes Simplex Virus Type 1 From Mice Lacking CD1d or NKT Cells Expressing the Semivariant Vα14-Jα281 TCR

Impaired Clearance of Herpes Simplex Virus Type 1 From Mice Lacking CD1d or NKT Cells Expressing the Semivariant Vα14-Jα281 TCR

CD4+ T cell migration into the cornea is reduced in CXCL9 deficient but not CXCL10 deficient mice following herpes simplex virus type 1 infection

DAP12 Signaling Directly Augments Proproliferative Cytokine Stimulation of NK Cells during Viral Infections

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