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Effects of interferon-beta on co-signaling molecules:upregulation of CD40, CD86 and PD-L2 on monocytes in relation to clinical response to interferon-beta treatment in patients with multiple sclerosis

Standard

Effects of interferon-beta on co-signaling molecules:upregulation of CD40, CD86 and PD-L2 on monocytes in relation to clinical response to interferon-beta treatment in patients with multiple sclerosis. / Wiesemann, Elke; Deb-Chatterji, Milani; Trebst, Corinna; Hemmer, Bernhard; Stangel, Martin; Windhagen, Anja.

In: MULT SCLER J, Vol. 14, No. 2, 03.2008, p. 166-76.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Wiesemann, E, Deb-Chatterji, M, Trebst, C, Hemmer, B, Stangel, M & Windhagen, A 2008, 'Effects of interferon-beta on co-signaling molecules:upregulation of CD40, CD86 and PD-L2 on monocytes in relation to clinical response to interferon-beta treatment in patients with multiple sclerosis', MULT SCLER J, vol. 14, no. 2, pp. 166-76. https://doi.org/10.1177/1352458507081342

APA

Wiesemann, E., Deb-Chatterji, M., Trebst, C., Hemmer, B., Stangel, M., & Windhagen, A. (2008). Effects of interferon-beta on co-signaling molecules:upregulation of CD40, CD86 and PD-L2 on monocytes in relation to clinical response to interferon-beta treatment in patients with multiple sclerosis. MULT SCLER J, 14(2), 166-76. https://doi.org/10.1177/1352458507081342

Vancouver

Wiesemann E, Deb-Chatterji M, Trebst C, Hemmer B, Stangel M, Windhagen A. Effects of interferon-beta on co-signaling molecules:upregulation of CD40, CD86 and PD-L2 on monocytes in relation to clinical response to interferon-beta treatment in patients with multiple sclerosis. MULT SCLER J. 2008 Mar;14(2):166-76. https://doi.org/10.1177/1352458507081342

Bibtex

@article{7f734571132740fabd027f571d1f3728,
title = "Effects of interferon-beta on co-signaling molecules:upregulation of CD40, CD86 and PD-L2 on monocytes in relation to clinical response to interferon-beta treatment in patients with multiple sclerosis",
abstract = "Interferon-beta (IFN-beta) reduces disease activity in a subgroup of patients with relapsing remitting multiple sclerosis (MS). The mechanism of action as well as the pathophysiological basis of responsiveness to IFN-beta is not well understood. Since T-cell activation plays an important part in the pathophysiology of MS, we here investigated the effect of IFN-beta on the expression of co-signaling pathways (CD28-CD80/CD86, CD154-CD40, ICOS-ICOSL, PD-1-PD-L1/2) in MS patients and correlated the results with the clinical response to IFN-beta in individual patients. Expression of co-signaling molecules was measured by flow cytometry in vitro on peripheral blood mononuclear cells after incubation with IFN-beta, and in vivo in whole blood samples of 32 untreated and 24 IFN-beta treated MS patients, including 13 patients longitudinal. IFN-beta treatment induced upregulation of CD40, CD80, CD86, PD-L1 and PD-L2 on monocytes as well as PD-L1 on CD4+-T-cells in vitro and in vivo. IFN-beta treated MS patients were grouped into responders and non-responders on the basis of Kurtzk{\'e}s EDSS (expanded disability status scale) progression and relapse rate. Upregulation of CD40, CD86 and PD-L2 on monocytes was associated with treatment response to IFN-beta (P < 0.001, P = 0.028 and P = 0.028, respectively). Our results show that IFN-beta upregulates co-stimulatory as well as co-inhibitory molecules in vitro and in vivo implicating that modulation of the balance between positive and negative co-stimulatory signals might be an important part of the mechanism of action of IFN-beta in MS. Upregulation of the expression of CD40, CD86 and PD-L2 may be useful as a predictive marker for clinical response to IFN-beta treatment at early timepoints during IFN-beta therapy.",
keywords = "Adult, Antibodies, Antigens, CD, Antigens, CD274, Antigens, CD40, Antigens, CD86, CD4-Positive T-Lymphocytes, Female, Flow Cytometry, Humans, Immunologic Factors, Intercellular Signaling Peptides and Proteins, Interferon-beta, Male, Middle Aged, Monocytes, Multiple Sclerosis, Relapsing-Remitting, Programmed Cell Death 1 Ligand 2 Protein, STAT1 Transcription Factor, Up-Regulation, Controlled Clinical Trial, Journal Article",
author = "Elke Wiesemann and Milani Deb-Chatterji and Corinna Trebst and Bernhard Hemmer and Martin Stangel and Anja Windhagen",
year = "2008",
month = mar,
doi = "10.1177/1352458507081342",
language = "English",
volume = "14",
pages = "166--76",
journal = "MULT SCLER J",
issn = "1352-4585",
publisher = "SAGE Publications",
number = "2",

}

RIS

TY - JOUR

T1 - Effects of interferon-beta on co-signaling molecules:upregulation of CD40, CD86 and PD-L2 on monocytes in relation to clinical response to interferon-beta treatment in patients with multiple sclerosis

AU - Wiesemann, Elke

AU - Deb-Chatterji, Milani

AU - Trebst, Corinna

AU - Hemmer, Bernhard

AU - Stangel, Martin

AU - Windhagen, Anja

PY - 2008/3

Y1 - 2008/3

N2 - Interferon-beta (IFN-beta) reduces disease activity in a subgroup of patients with relapsing remitting multiple sclerosis (MS). The mechanism of action as well as the pathophysiological basis of responsiveness to IFN-beta is not well understood. Since T-cell activation plays an important part in the pathophysiology of MS, we here investigated the effect of IFN-beta on the expression of co-signaling pathways (CD28-CD80/CD86, CD154-CD40, ICOS-ICOSL, PD-1-PD-L1/2) in MS patients and correlated the results with the clinical response to IFN-beta in individual patients. Expression of co-signaling molecules was measured by flow cytometry in vitro on peripheral blood mononuclear cells after incubation with IFN-beta, and in vivo in whole blood samples of 32 untreated and 24 IFN-beta treated MS patients, including 13 patients longitudinal. IFN-beta treatment induced upregulation of CD40, CD80, CD86, PD-L1 and PD-L2 on monocytes as well as PD-L1 on CD4+-T-cells in vitro and in vivo. IFN-beta treated MS patients were grouped into responders and non-responders on the basis of Kurtzkés EDSS (expanded disability status scale) progression and relapse rate. Upregulation of CD40, CD86 and PD-L2 on monocytes was associated with treatment response to IFN-beta (P < 0.001, P = 0.028 and P = 0.028, respectively). Our results show that IFN-beta upregulates co-stimulatory as well as co-inhibitory molecules in vitro and in vivo implicating that modulation of the balance between positive and negative co-stimulatory signals might be an important part of the mechanism of action of IFN-beta in MS. Upregulation of the expression of CD40, CD86 and PD-L2 may be useful as a predictive marker for clinical response to IFN-beta treatment at early timepoints during IFN-beta therapy.

AB - Interferon-beta (IFN-beta) reduces disease activity in a subgroup of patients with relapsing remitting multiple sclerosis (MS). The mechanism of action as well as the pathophysiological basis of responsiveness to IFN-beta is not well understood. Since T-cell activation plays an important part in the pathophysiology of MS, we here investigated the effect of IFN-beta on the expression of co-signaling pathways (CD28-CD80/CD86, CD154-CD40, ICOS-ICOSL, PD-1-PD-L1/2) in MS patients and correlated the results with the clinical response to IFN-beta in individual patients. Expression of co-signaling molecules was measured by flow cytometry in vitro on peripheral blood mononuclear cells after incubation with IFN-beta, and in vivo in whole blood samples of 32 untreated and 24 IFN-beta treated MS patients, including 13 patients longitudinal. IFN-beta treatment induced upregulation of CD40, CD80, CD86, PD-L1 and PD-L2 on monocytes as well as PD-L1 on CD4+-T-cells in vitro and in vivo. IFN-beta treated MS patients were grouped into responders and non-responders on the basis of Kurtzkés EDSS (expanded disability status scale) progression and relapse rate. Upregulation of CD40, CD86 and PD-L2 on monocytes was associated with treatment response to IFN-beta (P < 0.001, P = 0.028 and P = 0.028, respectively). Our results show that IFN-beta upregulates co-stimulatory as well as co-inhibitory molecules in vitro and in vivo implicating that modulation of the balance between positive and negative co-stimulatory signals might be an important part of the mechanism of action of IFN-beta in MS. Upregulation of the expression of CD40, CD86 and PD-L2 may be useful as a predictive marker for clinical response to IFN-beta treatment at early timepoints during IFN-beta therapy.

KW - Adult

KW - Antibodies

KW - Antigens, CD

KW - Antigens, CD274

KW - Antigens, CD40

KW - Antigens, CD86

KW - CD4-Positive T-Lymphocytes

KW - Female

KW - Flow Cytometry

KW - Humans

KW - Immunologic Factors

KW - Intercellular Signaling Peptides and Proteins

KW - Interferon-beta

KW - Male

KW - Middle Aged

KW - Monocytes

KW - Multiple Sclerosis, Relapsing-Remitting

KW - Programmed Cell Death 1 Ligand 2 Protein

KW - STAT1 Transcription Factor

KW - Up-Regulation

KW - Controlled Clinical Trial

KW - Journal Article

U2 - 10.1177/1352458507081342

DO - 10.1177/1352458507081342

M3 - SCORING: Journal article

C2 - 17942524

VL - 14

SP - 166

EP - 176

JO - MULT SCLER J

JF - MULT SCLER J

SN - 1352-4585

IS - 2

ER -