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",

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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

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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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