Functional maturation of proteolipid protein 139-151-specific Th1 cells in the central nervous system in experimental autoimmune encephalomyelitis

Mani Mohindru; Bongsu Kang; Byung S. Kim

doi:10.1016/j.jneuroim.2004.06.012

Functional maturation of proteolipid protein _139-151-specific Th1 cells in the central nervous system in experimental autoimmune encephalomyelitis

Mani Mohindru, Bongsu Kang, Byung S. Kim

Microbiology-Immunology

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

Abstract

Experimental autoimmune encephalomyelitis (EAE) is a widely adopted animal model system for studying human multiple sclerosis that affects the central nervous system (CNS). To understand the underlying pathogenic mechanisms of the autoimmune T cell response, localization, enumeration and characterization of autoreactive T cells are essential. We assessed encephalitogenic proteolipid protein epitope (PLP _139-151)-specific T cells in the periphery and CNS of SJL/J mice using MHC class II I-A ^s multimers during both pre-clinical and clinical phases of PLP-induced EAE in conjunction with T cell function. Our results strongly suggest that PLP _139-151-specific CD4 ⁺ T cells first expand primarily in the CNS-draining cervical lymph nodes and then migrate to the CNS. In the CNS, these PLP-specific CD4 ⁺ T cells accumulate, become activated and differentiate into effector cells that produce IFN-γ in response to the self-peptide.

Original language	English (US)
Pages (from-to)	127-135
Number of pages	9
Journal	Journal of Neuroimmunology
Volume	155
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2004.06.012
State	Published - Oct 2004

Funding

This work was supported by grants RO1 NS 28752 and RO1 NS 33008 from USPHS. We thank Drs. Ellis Reinherz and H.-C. Chang (Dana Farber Cancer Institute, Boston, MA) for LZ-containing plasmids, pCRII acid and pCRII base, Dr. Goldstein (Howard Hughes Medical Institute, La Jolla, CA) for insect cell expression vector, pRmHa-3 and Dr. V.K. Kuchroo (Harvard Medical School, Boston, MA) for 5B6 hybridoma.

Keywords

Autoimmunity
Class II tetramers
EAE/MS
MHC
T cell receptor

ASJC Scopus subject areas

Clinical Neurology
Neurology
Immunology and Allergy
Immunology

Access to Document

10.1016/j.jneuroim.2004.06.012

Cite this

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title = "Functional maturation of proteolipid protein 139-151-specific Th1 cells in the central nervous system in experimental autoimmune encephalomyelitis",

abstract = "Experimental autoimmune encephalomyelitis (EAE) is a widely adopted animal model system for studying human multiple sclerosis that affects the central nervous system (CNS). To understand the underlying pathogenic mechanisms of the autoimmune T cell response, localization, enumeration and characterization of autoreactive T cells are essential. We assessed encephalitogenic proteolipid protein epitope (PLP 139-151)-specific T cells in the periphery and CNS of SJL/J mice using MHC class II I-A s multimers during both pre-clinical and clinical phases of PLP-induced EAE in conjunction with T cell function. Our results strongly suggest that PLP 139-151-specific CD4 + T cells first expand primarily in the CNS-draining cervical lymph nodes and then migrate to the CNS. In the CNS, these PLP-specific CD4 + T cells accumulate, become activated and differentiate into effector cells that produce IFN-γ in response to the self-peptide.",

keywords = "Autoimmunity, Class II tetramers, EAE/MS, MHC, T cell receptor",

author = "Mani Mohindru and Bongsu Kang and Kim, {Byung S.}",

note = "Funding Information: This work was supported by grants RO1 NS 28752 and RO1 NS 33008 from USPHS. We thank Drs. Ellis Reinherz and H.-C. Chang (Dana Farber Cancer Institute, Boston, MA) for LZ-containing plasmids, pCRII acid and pCRII base, Dr. Goldstein (Howard Hughes Medical Institute, La Jolla, CA) for insect cell expression vector, pRmHa-3 and Dr. V.K. Kuchroo (Harvard Medical School, Boston, MA) for 5B6 hybridoma.",

year = "2004",

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language = "English (US)",

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AU - Mohindru, Mani

AU - Kang, Bongsu

AU - Kim, Byung S.

N1 - Funding Information: This work was supported by grants RO1 NS 28752 and RO1 NS 33008 from USPHS. We thank Drs. Ellis Reinherz and H.-C. Chang (Dana Farber Cancer Institute, Boston, MA) for LZ-containing plasmids, pCRII acid and pCRII base, Dr. Goldstein (Howard Hughes Medical Institute, La Jolla, CA) for insect cell expression vector, pRmHa-3 and Dr. V.K. Kuchroo (Harvard Medical School, Boston, MA) for 5B6 hybridoma.

PY - 2004/10

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N2 - Experimental autoimmune encephalomyelitis (EAE) is a widely adopted animal model system for studying human multiple sclerosis that affects the central nervous system (CNS). To understand the underlying pathogenic mechanisms of the autoimmune T cell response, localization, enumeration and characterization of autoreactive T cells are essential. We assessed encephalitogenic proteolipid protein epitope (PLP 139-151)-specific T cells in the periphery and CNS of SJL/J mice using MHC class II I-A s multimers during both pre-clinical and clinical phases of PLP-induced EAE in conjunction with T cell function. Our results strongly suggest that PLP 139-151-specific CD4 + T cells first expand primarily in the CNS-draining cervical lymph nodes and then migrate to the CNS. In the CNS, these PLP-specific CD4 + T cells accumulate, become activated and differentiate into effector cells that produce IFN-γ in response to the self-peptide.

AB - Experimental autoimmune encephalomyelitis (EAE) is a widely adopted animal model system for studying human multiple sclerosis that affects the central nervous system (CNS). To understand the underlying pathogenic mechanisms of the autoimmune T cell response, localization, enumeration and characterization of autoreactive T cells are essential. We assessed encephalitogenic proteolipid protein epitope (PLP 139-151)-specific T cells in the periphery and CNS of SJL/J mice using MHC class II I-A s multimers during both pre-clinical and clinical phases of PLP-induced EAE in conjunction with T cell function. Our results strongly suggest that PLP 139-151-specific CD4 + T cells first expand primarily in the CNS-draining cervical lymph nodes and then migrate to the CNS. In the CNS, these PLP-specific CD4 + T cells accumulate, become activated and differentiate into effector cells that produce IFN-γ in response to the self-peptide.

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