Memory B cells from a subset of treatment-naïve relapsing-remitting multiple sclerosis patients elicit CD4+ T-cell proliferation and IFN-γ production in response to myelin basic protein and myelin oligodendrocyte glycoprotein

Research output: Contribution to journalArticle

Christopher T. Harp, Sara Ireland, Laurie S. Davis, Gina Remington, Bonnie Cassidy, Petra D. Cravens, Olaf Stuve, Amy E. Lovett-Racke, Todd N. Eagar, Benjamin M. Greenberg, Michael K. Racke, Lindsay G. Cowell, Nitin J. Karandikar, Elliot M. Frohman, Nancy L. Monson

Recent evidence suggests that B- and T-cell interactions may be paramount in relapsingremitting MS (RRMS) disease pathogenesis. We hypothesized that memory B-cell pools from RRMS patients may specifically harbor a subset of potent neuro-APC that support neuro-Ag reactive T-cell proliferation and cytokine secretion. To test this hypothesis, we compared CD80 and HLA-DR expression, IL-10 and lymphotoxin-α secretion, neuro-Ag binding capacity, and neuro-Ag presentation by memory B cells from RRMS patients to naïve B cells from RRMS patients and to memory and naïve B cells from healthy donors (HD). We identified memory B cells from some RRMS patients that elicited CD4+ T-cell proliferation and IFN-γ secretion in response to myelin basic protein and myelin oligodendrocyte glycoprotein. Notwithstanding the fact that the phenotypic parameters that promote efficient Ag presentation were observed to be similar between RRMS and HD memory B cells, a corresponding capability to elicit CD4+ T-cell proliferation in response to myelin basic protein and myelin oligodendrocyte glycoprotein was not observed in HD memory B cells. Our results demonstrate for the first time that the memory B-cell pool in RRMS harbors neuro-Ag specific B cells that can activate T cells.

Original languageEnglish (US)
Pages (from-to)2942-2956
Number of pages15
JournalEuropean Journal of Immunology
Volume40
Issue number10
DOIs
StatePublished - Oct 1 2010

PMID: 20812237

PMCID: PMC3072802

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Memory B cells from a subset of treatment-naïve relapsing-remitting multiple sclerosis patients elicit CD4+ T-cell proliferation and IFN-γ production in response to myelin basic protein and myelin oligodendrocyte glycoprotein. / Harp, Christopher T.; Ireland, Sara; Davis, Laurie S.; Remington, Gina; Cassidy, Bonnie; Cravens, Petra D.; Stuve, Olaf; Lovett-Racke, Amy E.; Eagar, Todd N.; Greenberg, Benjamin M.; Racke, Michael K.; Cowell, Lindsay G.; Karandikar, Nitin J.; Frohman, Elliot M.; Monson, Nancy L.

In: European Journal of Immunology, Vol. 40, No. 10, 01.10.2010, p. 2942-2956.

Research output: Contribution to journalArticle

Harvard

Harp, CT, Ireland, S, Davis, LS, Remington, G, Cassidy, B, Cravens, PD, Stuve, O, Lovett-Racke, AE, Eagar, TN, Greenberg, BM, Racke, MK, Cowell, LG, Karandikar, NJ, Frohman, EM & Monson, NL 2010, 'Memory B cells from a subset of treatment-naïve relapsing-remitting multiple sclerosis patients elicit CD4+ T-cell proliferation and IFN-γ production in response to myelin basic protein and myelin oligodendrocyte glycoprotein' European Journal of Immunology, vol. 40, no. 10, pp. 2942-2956. https://doi.org/10.1002/eji.201040516

APA

Harp, C. T., Ireland, S., Davis, L. S., Remington, G., Cassidy, B., Cravens, P. D., ... Monson, N. L. (2010). Memory B cells from a subset of treatment-naïve relapsing-remitting multiple sclerosis patients elicit CD4+ T-cell proliferation and IFN-γ production in response to myelin basic protein and myelin oligodendrocyte glycoprotein. European Journal of Immunology, 40(10), 2942-2956. https://doi.org/10.1002/eji.201040516

Vancouver

Harp CT, Ireland S, Davis LS, Remington G, Cassidy B, Cravens PD et al. Memory B cells from a subset of treatment-naïve relapsing-remitting multiple sclerosis patients elicit CD4+ T-cell proliferation and IFN-γ production in response to myelin basic protein and myelin oligodendrocyte glycoprotein. European Journal of Immunology. 2010 Oct 1;40(10):2942-2956. https://doi.org/10.1002/eji.201040516

Author

Harp, Christopher T. ; Ireland, Sara ; Davis, Laurie S. ; Remington, Gina ; Cassidy, Bonnie ; Cravens, Petra D. ; Stuve, Olaf ; Lovett-Racke, Amy E. ; Eagar, Todd N. ; Greenberg, Benjamin M. ; Racke, Michael K. ; Cowell, Lindsay G. ; Karandikar, Nitin J. ; Frohman, Elliot M. ; Monson, Nancy L. / Memory B cells from a subset of treatment-naïve relapsing-remitting multiple sclerosis patients elicit CD4+ T-cell proliferation and IFN-γ production in response to myelin basic protein and myelin oligodendrocyte glycoprotein. In: European Journal of Immunology. 2010 ; Vol. 40, No. 10. pp. 2942-2956.

BibTeX

@article{91f6592f54fb4668a57225b754c939f5,
title = "Memory B cells from a subset of treatment-na{\"i}ve relapsing-remitting multiple sclerosis patients elicit CD4+ T-cell proliferation and IFN-γ production in response to myelin basic protein and myelin oligodendrocyte glycoprotein",
abstract = "Recent evidence suggests that B- and T-cell interactions may be paramount in relapsingremitting MS (RRMS) disease pathogenesis. We hypothesized that memory B-cell pools from RRMS patients may specifically harbor a subset of potent neuro-APC that support neuro-Ag reactive T-cell proliferation and cytokine secretion. To test this hypothesis, we compared CD80 and HLA-DR expression, IL-10 and lymphotoxin-α secretion, neuro-Ag binding capacity, and neuro-Ag presentation by memory B cells from RRMS patients to na{\"i}ve B cells from RRMS patients and to memory and na{\"i}ve B cells from healthy donors (HD). We identified memory B cells from some RRMS patients that elicited CD4+ T-cell proliferation and IFN-γ secretion in response to myelin basic protein and myelin oligodendrocyte glycoprotein. Notwithstanding the fact that the phenotypic parameters that promote efficient Ag presentation were observed to be similar between RRMS and HD memory B cells, a corresponding capability to elicit CD4+ T-cell proliferation in response to myelin basic protein and myelin oligodendrocyte glycoprotein was not observed in HD memory B cells. Our results demonstrate for the first time that the memory B-cell pool in RRMS harbors neuro-Ag specific B cells that can activate T cells.",
keywords = "Ag presentation, Autoimmunity, B cells, MS",
author = "Harp, {Christopher T.} and Sara Ireland and Davis, {Laurie S.} and Gina Remington and Bonnie Cassidy and Cravens, {Petra D.} and Olaf Stuve and Lovett-Racke, {Amy E.} and Eagar, {Todd N.} and Greenberg, {Benjamin M.} and Racke, {Michael K.} and Cowell, {Lindsay G.} and Karandikar, {Nitin J.} and Frohman, {Elliot M.} and Monson, {Nancy L.}",
year = "2010",
month = "10",
day = "1",
doi = "10.1002/eji.201040516",
language = "English (US)",
volume = "40",
pages = "2942--2956",
journal = "European Journal of Immunology",
issn = "0014-2980",
publisher = "Wiley",
number = "10",

}

RIS

TY - JOUR

T1 - Memory B cells from a subset of treatment-naïve relapsing-remitting multiple sclerosis patients elicit CD4+ T-cell proliferation and IFN-γ production in response to myelin basic protein and myelin oligodendrocyte glycoprotein

AU - Harp, Christopher T.

AU - Ireland, Sara

AU - Davis, Laurie S.

AU - Remington, Gina

AU - Cassidy, Bonnie

AU - Cravens, Petra D.

AU - Stuve, Olaf

AU - Lovett-Racke, Amy E.

AU - Eagar, Todd N.

AU - Greenberg, Benjamin M.

AU - Racke, Michael K.

AU - Cowell, Lindsay G.

AU - Karandikar, Nitin J.

AU - Frohman, Elliot M.

AU - Monson, Nancy L.

PY - 2010/10/1

Y1 - 2010/10/1

N2 - Recent evidence suggests that B- and T-cell interactions may be paramount in relapsingremitting MS (RRMS) disease pathogenesis. We hypothesized that memory B-cell pools from RRMS patients may specifically harbor a subset of potent neuro-APC that support neuro-Ag reactive T-cell proliferation and cytokine secretion. To test this hypothesis, we compared CD80 and HLA-DR expression, IL-10 and lymphotoxin-α secretion, neuro-Ag binding capacity, and neuro-Ag presentation by memory B cells from RRMS patients to naïve B cells from RRMS patients and to memory and naïve B cells from healthy donors (HD). We identified memory B cells from some RRMS patients that elicited CD4+ T-cell proliferation and IFN-γ secretion in response to myelin basic protein and myelin oligodendrocyte glycoprotein. Notwithstanding the fact that the phenotypic parameters that promote efficient Ag presentation were observed to be similar between RRMS and HD memory B cells, a corresponding capability to elicit CD4+ T-cell proliferation in response to myelin basic protein and myelin oligodendrocyte glycoprotein was not observed in HD memory B cells. Our results demonstrate for the first time that the memory B-cell pool in RRMS harbors neuro-Ag specific B cells that can activate T cells.

AB - Recent evidence suggests that B- and T-cell interactions may be paramount in relapsingremitting MS (RRMS) disease pathogenesis. We hypothesized that memory B-cell pools from RRMS patients may specifically harbor a subset of potent neuro-APC that support neuro-Ag reactive T-cell proliferation and cytokine secretion. To test this hypothesis, we compared CD80 and HLA-DR expression, IL-10 and lymphotoxin-α secretion, neuro-Ag binding capacity, and neuro-Ag presentation by memory B cells from RRMS patients to naïve B cells from RRMS patients and to memory and naïve B cells from healthy donors (HD). We identified memory B cells from some RRMS patients that elicited CD4+ T-cell proliferation and IFN-γ secretion in response to myelin basic protein and myelin oligodendrocyte glycoprotein. Notwithstanding the fact that the phenotypic parameters that promote efficient Ag presentation were observed to be similar between RRMS and HD memory B cells, a corresponding capability to elicit CD4+ T-cell proliferation in response to myelin basic protein and myelin oligodendrocyte glycoprotein was not observed in HD memory B cells. Our results demonstrate for the first time that the memory B-cell pool in RRMS harbors neuro-Ag specific B cells that can activate T cells.

KW - Ag presentation

KW - Autoimmunity

KW - B cells

KW - MS

UR - http://www.scopus.com/inward/record.url?scp=77957126531&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77957126531&partnerID=8YFLogxK

U2 - 10.1002/eji.201040516

DO - 10.1002/eji.201040516

M3 - Article

VL - 40

SP - 2942

EP - 2956

JO - European Journal of Immunology

T2 - European Journal of Immunology

JF - European Journal of Immunology

SN - 0014-2980

IS - 10

ER -

ID: 16810620