(p40)2-Fc reduces immune-inflammatory response through the activation of T cells in collagen induced arthritis mice

Seon Yeong Lee; Seung Hoon Lee; Seong Jeong Park; Doo Jin Kim; Eun Kyung Kim; Jae Kyung Kim; Se Hwan Yang; Sung Hwan Park; Young Chul Sung; Ho Youn Kim; Mi La Cho

doi:10.1016/j.imlet.2016.05.013

(p40)2-Fc reduces immune-inflammatory response through the activation of T cells in collagen induced arthritis mice

Seon Yeong Lee
, Seung Hoon Lee
, Seong Jeong Park
, Doo Jin Kim
, Eun Kyung Kim
, Jae Kyung Kim
, Se Hwan Yang
, Sung Hwan Park
, Young Chul Sung
, Ho Youn Kim
, Mi La Cho

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

2 Scopus citations

Abstract

IL-12p40 homodimer, a natural antagonist of IL-12 and IL-23, performs an important role in the expression of proinflammatory cytokines that is essential for Th1 and Th17 immune responses. Here, we reveal the therapeutic and immunosuppressive effect of the IL-12p40 subunit ((p40)₂-Fc) in an experimental autoimmune arthritis model. We hypothesized that (p40)₂-Fc may reduce the inflammatory response and the activation of T cells. In this study, we intraperitoneally injected (p40)₂-Fc into collagen induced arthritis (CIA) mice to identify whether (p40)₂-Fc attenuates CIA severity. (p40)₂-Fc reduced the development of CIA, joint inflammation and cartilage destruction. (p40)₂-Fc also significantly decreased the concentration of serum immunoglobulin as well as the number of T cells and C II specific T cells. In addition, osteoclastogenesis in (p40)₂-Fc treated mice was down-regulated compared to the mice treated with (p40)₂-Fc control. We observed that (p40)₂-Fc treatment alleviates arthritis in mice with CIA, reducing inflammation and osteoclast differentiation. These findings suggest that (p40)₂-Fc can be a potential therapeutic approach for autoimmune arthritis.

Original language	English
Pages (from-to)	36-43
Number of pages	8
Journal	Immunology Letters
Volume	176
DOIs	https://doi.org/10.1016/j.imlet.2016.05.013
State	Published - 1 Aug 2016

Bibliographical note

Publisher Copyright:
© 2016 European Federation of Immunological Societies.

Keywords

(p40)2-Fc
Osteoclastogenesis
Rheumatoid arthritis

Access to Document

10.1016/j.imlet.2016.05.013

Cite this

@article{53cc74234ff64cb3868ccc9d35eddee1,

title = "(p40)2-Fc reduces immune-inflammatory response through the activation of T cells in collagen induced arthritis mice",

abstract = "IL-12p40 homodimer, a natural antagonist of IL-12 and IL-23, performs an important role in the expression of proinflammatory cytokines that is essential for Th1 and Th17 immune responses. Here, we reveal the therapeutic and immunosuppressive effect of the IL-12p40 subunit ((p40)2-Fc) in an experimental autoimmune arthritis model. We hypothesized that (p40)2-Fc may reduce the inflammatory response and the activation of T cells. In this study, we intraperitoneally injected (p40)2-Fc into collagen induced arthritis (CIA) mice to identify whether (p40)2-Fc attenuates CIA severity. (p40)2-Fc reduced the development of CIA, joint inflammation and cartilage destruction. (p40)2-Fc also significantly decreased the concentration of serum immunoglobulin as well as the number of T cells and C II specific T cells. In addition, osteoclastogenesis in (p40)2-Fc treated mice was down-regulated compared to the mice treated with (p40)2-Fc control. We observed that (p40)2-Fc treatment alleviates arthritis in mice with CIA, reducing inflammation and osteoclast differentiation. These findings suggest that (p40)2-Fc can be a potential therapeutic approach for autoimmune arthritis.",

keywords = "(p40)2-Fc, Osteoclastogenesis, Rheumatoid arthritis",

author = "Lee, \{Seon Yeong\} and Lee, \{Seung Hoon\} and Park, \{Seong Jeong\} and Kim, \{Doo Jin\} and Kim, \{Eun Kyung\} and Kim, \{Jae Kyung\} and Yang, \{Se Hwan\} and Park, \{Sung Hwan\} and Sung, \{Young Chul\} and Kim, \{Ho Youn\} and Cho, \{Mi La\}",

note = "Publisher Copyright: {\textcopyright} 2016 European Federation of Immunological Societies.",

year = "2016",

month = aug,

day = "1",

doi = "10.1016/j.imlet.2016.05.013",

language = "English",

volume = "176",

pages = "36--43",

journal = "Immunology Letters",

issn = "0165-2478",

publisher = "Elsevier B.V.",

}

TY - JOUR

T1 - (p40)2-Fc reduces immune-inflammatory response through the activation of T cells in collagen induced arthritis mice

AU - Lee, Seon Yeong

AU - Lee, Seung Hoon

AU - Park, Seong Jeong

AU - Kim, Doo Jin

AU - Kim, Eun Kyung

AU - Kim, Jae Kyung

AU - Yang, Se Hwan

AU - Park, Sung Hwan

AU - Sung, Young Chul

AU - Kim, Ho Youn

AU - Cho, Mi La

PY - 2016/8/1

Y1 - 2016/8/1

N2 - IL-12p40 homodimer, a natural antagonist of IL-12 and IL-23, performs an important role in the expression of proinflammatory cytokines that is essential for Th1 and Th17 immune responses. Here, we reveal the therapeutic and immunosuppressive effect of the IL-12p40 subunit ((p40)2-Fc) in an experimental autoimmune arthritis model. We hypothesized that (p40)2-Fc may reduce the inflammatory response and the activation of T cells. In this study, we intraperitoneally injected (p40)2-Fc into collagen induced arthritis (CIA) mice to identify whether (p40)2-Fc attenuates CIA severity. (p40)2-Fc reduced the development of CIA, joint inflammation and cartilage destruction. (p40)2-Fc also significantly decreased the concentration of serum immunoglobulin as well as the number of T cells and C II specific T cells. In addition, osteoclastogenesis in (p40)2-Fc treated mice was down-regulated compared to the mice treated with (p40)2-Fc control. We observed that (p40)2-Fc treatment alleviates arthritis in mice with CIA, reducing inflammation and osteoclast differentiation. These findings suggest that (p40)2-Fc can be a potential therapeutic approach for autoimmune arthritis.

AB - IL-12p40 homodimer, a natural antagonist of IL-12 and IL-23, performs an important role in the expression of proinflammatory cytokines that is essential for Th1 and Th17 immune responses. Here, we reveal the therapeutic and immunosuppressive effect of the IL-12p40 subunit ((p40)2-Fc) in an experimental autoimmune arthritis model. We hypothesized that (p40)2-Fc may reduce the inflammatory response and the activation of T cells. In this study, we intraperitoneally injected (p40)2-Fc into collagen induced arthritis (CIA) mice to identify whether (p40)2-Fc attenuates CIA severity. (p40)2-Fc reduced the development of CIA, joint inflammation and cartilage destruction. (p40)2-Fc also significantly decreased the concentration of serum immunoglobulin as well as the number of T cells and C II specific T cells. In addition, osteoclastogenesis in (p40)2-Fc treated mice was down-regulated compared to the mice treated with (p40)2-Fc control. We observed that (p40)2-Fc treatment alleviates arthritis in mice with CIA, reducing inflammation and osteoclast differentiation. These findings suggest that (p40)2-Fc can be a potential therapeutic approach for autoimmune arthritis.

KW - (p40)2-Fc

KW - Osteoclastogenesis

KW - Rheumatoid arthritis

UR - https://www.scopus.com/pages/publications/84973169215

U2 - 10.1016/j.imlet.2016.05.013

DO - 10.1016/j.imlet.2016.05.013

M3 - Article

C2 - 27229912

AN - SCOPUS:84973169215

SN - 0165-2478

VL - 176

SP - 36

EP - 43

JO - Immunology Letters

JF - Immunology Letters

ER -

(p40)2-Fc reduces immune-inflammatory response through the activation of T cells in collagen induced arthritis mice

Abstract

Bibliographical note

Keywords

Access to Document

Other files and links

Fingerprint

Cite this