NOS2 regulates cytokine production and VLA-4 expression in experimental autoimmune encephalomyelitis

Anne H. Cross; Michael J. Ramsbottom; Jeri Anne Lyons

doi:10.1016/j.jneuroim.2005.11.022

NOS2 regulates cytokine production and VLA-4 expression in experimental autoimmune encephalomyelitis

Anne H. Cross, Michael J. Ramsbottom, Jeri Anne Lyons

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9 Scopus citations

Abstract

Inducible nitric oxide synthase (NOS2) expression in the central nervous system correlates with EAE disease activity. Inhibition of NOS2 ameliorates adoptively transferred EAE, yet exacerbates actively induced EAE. Herein, the encephalitogenicity of T cells induced by immunization in the presence or absence of NOS2 was examined. Upon passive transfer, T cells from myelin oligodendrocyte glycoprotein-immunized NOS2-deficient C57BL/6 mice induced more severe EAE than T cells from wild-type mice. The heightened encephalitogenicity of NOS2-/- T cells correlated with enhanced expression of VLA-4 (CD49d) and increased production of interferon gamma and tumor necrosis factor. NO plays an important regulatory role in autoimmune T cell induction.

Original language	English
Pages (from-to)	79-86
Number of pages	8
Journal	Journal of Neuroimmunology
Volume	173
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2005.11.022
State	Published - Apr 2006

Keywords

Experimental autoimmune encephalomyelitis
Immune regulation
Interferon gamma
Nitric oxide
Tumor necrosis factor-alpha
VLA-4

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10.1016/j.jneuroim.2005.11.022

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title = "NOS2 regulates cytokine production and VLA-4 expression in experimental autoimmune encephalomyelitis",

abstract = "Inducible nitric oxide synthase (NOS2) expression in the central nervous system correlates with EAE disease activity. Inhibition of NOS2 ameliorates adoptively transferred EAE, yet exacerbates actively induced EAE. Herein, the encephalitogenicity of T cells induced by immunization in the presence or absence of NOS2 was examined. Upon passive transfer, T cells from myelin oligodendrocyte glycoprotein-immunized NOS2-deficient C57BL/6 mice induced more severe EAE than T cells from wild-type mice. The heightened encephalitogenicity of NOS2-/- T cells correlated with enhanced expression of VLA-4 (CD49d) and increased production of interferon gamma and tumor necrosis factor. NO plays an important regulatory role in autoimmune T cell induction.",

keywords = "Experimental autoimmune encephalomyelitis, Immune regulation, Interferon gamma, Nitric oxide, Tumor necrosis factor-alpha, VLA-4",

author = "Cross, {Anne H.} and Ramsbottom, {Michael J.} and Lyons, {Jeri Anne}",

note = "Funding Information: This work was supported by the National Institutes of Health Grant RO1 NS37037 (to AHC). JAL was a Fellow of the National Multiple Sclerosis Society (FG-1259) during some of these studies. We thank Drs. John L. Trotter (deceased), John H. Russell, Thomas P. Misko, Jennifer Stark and Kimberly Sabelko for helpful discussion and Manuel San for technical assistance.",

year = "2006",

month = apr,

doi = "10.1016/j.jneuroim.2005.11.022",

language = "English",

volume = "173",

pages = "79--86",

journal = "Journal of Neuroimmunology",

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T1 - NOS2 regulates cytokine production and VLA-4 expression in experimental autoimmune encephalomyelitis

AU - Cross, Anne H.

AU - Ramsbottom, Michael J.

AU - Lyons, Jeri Anne

N1 - Funding Information: This work was supported by the National Institutes of Health Grant RO1 NS37037 (to AHC). JAL was a Fellow of the National Multiple Sclerosis Society (FG-1259) during some of these studies. We thank Drs. John L. Trotter (deceased), John H. Russell, Thomas P. Misko, Jennifer Stark and Kimberly Sabelko for helpful discussion and Manuel San for technical assistance.

PY - 2006/4

Y1 - 2006/4

N2 - Inducible nitric oxide synthase (NOS2) expression in the central nervous system correlates with EAE disease activity. Inhibition of NOS2 ameliorates adoptively transferred EAE, yet exacerbates actively induced EAE. Herein, the encephalitogenicity of T cells induced by immunization in the presence or absence of NOS2 was examined. Upon passive transfer, T cells from myelin oligodendrocyte glycoprotein-immunized NOS2-deficient C57BL/6 mice induced more severe EAE than T cells from wild-type mice. The heightened encephalitogenicity of NOS2-/- T cells correlated with enhanced expression of VLA-4 (CD49d) and increased production of interferon gamma and tumor necrosis factor. NO plays an important regulatory role in autoimmune T cell induction.

AB - Inducible nitric oxide synthase (NOS2) expression in the central nervous system correlates with EAE disease activity. Inhibition of NOS2 ameliorates adoptively transferred EAE, yet exacerbates actively induced EAE. Herein, the encephalitogenicity of T cells induced by immunization in the presence or absence of NOS2 was examined. Upon passive transfer, T cells from myelin oligodendrocyte glycoprotein-immunized NOS2-deficient C57BL/6 mice induced more severe EAE than T cells from wild-type mice. The heightened encephalitogenicity of NOS2-/- T cells correlated with enhanced expression of VLA-4 (CD49d) and increased production of interferon gamma and tumor necrosis factor. NO plays an important regulatory role in autoimmune T cell induction.

KW - Experimental autoimmune encephalomyelitis

KW - Immune regulation

KW - Interferon gamma

KW - Nitric oxide

KW - Tumor necrosis factor-alpha

KW - VLA-4

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U2 - 10.1016/j.jneuroim.2005.11.022

DO - 10.1016/j.jneuroim.2005.11.022

M3 - Article

C2 - 16448705

AN - SCOPUS:33644963786

SN - 0165-5728

VL - 173

SP - 79

EP - 86

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

IS - 1-2

ER -

NOS2 regulates cytokine production and VLA-4 expression in experimental autoimmune encephalomyelitis

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Keywords

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