In trans T cell tolerance exacerbates experimental allergic encephalomyelitis by interfering with protective antibody responses

Jason A. Cascio; Marie Therese Khairallah; Xiaoxiao Wan; Weirong Chen; Linda M. Rowland; Mermagya Dhakal; Mindy M. Miller; Habib Zaghouani

doi:10.1016/j.jneuroim.2013.09.022

In trans T cell tolerance exacerbates experimental allergic encephalomyelitis by interfering with protective antibody responses

Jason A. Cascio
, Marie Therese Khairallah
, Xiaoxiao Wan
, Weirong Chen
, Linda M. Rowland
, Mermagya Dhakal
, Mindy M. Miller
, Habib Zaghouani

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

1 Scopus citations

Abstract

F₁ (SJL/J×C57BL/6) mice with MOG35-55-induced EAE recover from disease when treated with Ig-MOG carrying MOG35-55 peptide. However, Ig-PLP1, carrying PLP139-151, induced reduction of anti-MOG antibodies and exacerbated EAE. Herein, we show that Ig-PLP1 specifically reduces the frequency of B cells producing protective IgG2a/b anti-MOG antibodies. Surprisingly, these cells were marginal zone (MZ), rather than follicular (FO) or newly formed (NF), B cells and transfer of MZ B cells into sick mice nullified disease exacerbation by Ig-PLP1 in a complement dependent manner. These findings reveal a potential self-limiting regulatory mechanism involving auto-antibodies in MOG EAE.

Original language	English
Pages (from-to)	49-55
Number of pages	7
Journal	Journal of Neuroimmunology
Volume	266
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2013.09.022
State	Published - Jan 15 2014

Keywords

Anti-MOG antibodies
Autoimmunity
B cells
EAE
T cell tolerance

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10.1016/j.jneuroim.2013.09.022

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@article{80e6803956bc4badbda61e62cc861b6e,

title = "In trans T cell tolerance exacerbates experimental allergic encephalomyelitis by interfering with protective antibody responses",

abstract = "F1 (SJL/J×C57BL/6) mice with MOG35-55-induced EAE recover from disease when treated with Ig-MOG carrying MOG35-55 peptide. However, Ig-PLP1, carrying PLP139-151, induced reduction of anti-MOG antibodies and exacerbated EAE. Herein, we show that Ig-PLP1 specifically reduces the frequency of B cells producing protective IgG2a/b anti-MOG antibodies. Surprisingly, these cells were marginal zone (MZ), rather than follicular (FO) or newly formed (NF), B cells and transfer of MZ B cells into sick mice nullified disease exacerbation by Ig-PLP1 in a complement dependent manner. These findings reveal a potential self-limiting regulatory mechanism involving auto-antibodies in MOG EAE.",

keywords = "Anti-MOG antibodies, Autoimmunity, B cells, EAE, T cell tolerance",

author = "Cascio, \{Jason A.\} and Khairallah, \{Marie Therese\} and Xiaoxiao Wan and Weirong Chen and Rowland, \{Linda M.\} and Mermagya Dhakal and Miller, \{Mindy M.\} and Habib Zaghouani",

note = "Funding Information: This work was supported by grants RO1 NS057194 (to H.Z.) from the National Institutes of Health , and by the J. Lavenia Edwards endowment (to HZ).",

year = "2014",

month = jan,

day = "15",

doi = "10.1016/j.jneuroim.2013.09.022",

language = "English",

volume = "266",

pages = "49--55",

journal = "Journal of Neuroimmunology",

issn = "0165-5728",

number = "1-2",

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TY - JOUR

T1 - In trans T cell tolerance exacerbates experimental allergic encephalomyelitis by interfering with protective antibody responses

AU - Cascio, Jason A.

AU - Khairallah, Marie Therese

AU - Wan, Xiaoxiao

AU - Chen, Weirong

AU - Rowland, Linda M.

AU - Dhakal, Mermagya

AU - Miller, Mindy M.

AU - Zaghouani, Habib

N1 - Funding Information: This work was supported by grants RO1 NS057194 (to H.Z.) from the National Institutes of Health , and by the J. Lavenia Edwards endowment (to HZ).

PY - 2014/1/15

Y1 - 2014/1/15

N2 - F1 (SJL/J×C57BL/6) mice with MOG35-55-induced EAE recover from disease when treated with Ig-MOG carrying MOG35-55 peptide. However, Ig-PLP1, carrying PLP139-151, induced reduction of anti-MOG antibodies and exacerbated EAE. Herein, we show that Ig-PLP1 specifically reduces the frequency of B cells producing protective IgG2a/b anti-MOG antibodies. Surprisingly, these cells were marginal zone (MZ), rather than follicular (FO) or newly formed (NF), B cells and transfer of MZ B cells into sick mice nullified disease exacerbation by Ig-PLP1 in a complement dependent manner. These findings reveal a potential self-limiting regulatory mechanism involving auto-antibodies in MOG EAE.

AB - F1 (SJL/J×C57BL/6) mice with MOG35-55-induced EAE recover from disease when treated with Ig-MOG carrying MOG35-55 peptide. However, Ig-PLP1, carrying PLP139-151, induced reduction of anti-MOG antibodies and exacerbated EAE. Herein, we show that Ig-PLP1 specifically reduces the frequency of B cells producing protective IgG2a/b anti-MOG antibodies. Surprisingly, these cells were marginal zone (MZ), rather than follicular (FO) or newly formed (NF), B cells and transfer of MZ B cells into sick mice nullified disease exacerbation by Ig-PLP1 in a complement dependent manner. These findings reveal a potential self-limiting regulatory mechanism involving auto-antibodies in MOG EAE.

KW - Anti-MOG antibodies

KW - Autoimmunity

KW - B cells

KW - EAE

KW - T cell tolerance

UR - https://www.scopus.com/pages/publications/84891496251

U2 - 10.1016/j.jneuroim.2013.09.022

DO - 10.1016/j.jneuroim.2013.09.022

M3 - Article

C2 - 24196276

AN - SCOPUS:84891496251

SN - 0165-5728

VL - 266

SP - 49

EP - 55

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

IS - 1-2

ER -

In trans T cell tolerance exacerbates experimental allergic encephalomyelitis by interfering with protective antibody responses

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Keywords

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