IFNγ deficient C57BL/6 (H-2b) mice develop collagen induced arthritis with predominant usage of T cell receptor Vβ6 and Vβ8 in arthritic joints

Cong-Qiu Chu, Z. Song, L. Mayton, B. Wu, P. H. Wooley

Research output: Contribution to journalArticle

56 Citations (Scopus)

Abstract

Background: Transgenic deficiency in interferon γ (IFNγ) or IFNγ receptor makes resistant strains of mice bearing H-2b or H-2d susceptible to collagen induced arthritis (CIA). Objective: To determine whether the escape from regulation of disease susceptibility at the major histocompatibility complex level involves a new use of autoimmune T cells expressing T cell receptor (TCR) Vβ that vary from the cell populations previously identified within arthritic joints. Methods: Arthritis was induced by a standard protocol with type II bovine collagen (CII) in complete Freund's adjuvant. Clinical features, histopathology, immunological responses, and TCR profile in arthritic joints in IFNγ knockout C57BL/6 (B6.IFNγ KO) mice (H-2b) were compared directly with those in DBA/1 mice (H-2 q). Results: 60-80% of B6.IFNγ KO mice developed a progressive arthritis with a similar clinical course to classical CIA in DBA/1 mice. The affected joints in B6.IFNγ KO mice had an erosive form of arthritis with similar features to joint disease in DBA/1 mice. B6.IFNγ KO mice produced significantly higher levels of IgG2b and IgG1 autoantibodies to murine CII and showed increased proliferative response to CII compared with B6 mice. Comparable levels of interleukin 1β and tumour necrosis factor α expression were detected in arthritic joints from B6.IFNγ KO and DBA/1 mice. B6.IFNγKO mice used predominantly TCR Vβ6 and Vβ8 in arthritic joints. This TCR Vβ profile is similar to that found in DBA/1 mice with CIA. Conclusions: C57BL/6 mice deficient in IFNγ production can develop arthritis that resembles classical CIA. These data suggest that IFNγ is a key factor mediating susceptibility to CIA.

Original languageEnglish (US)
Pages (from-to)983-990
Number of pages8
JournalAnnals of the Rheumatic Diseases
Volume62
Issue number10
DOIs
StatePublished - Oct 1 2003
Externally publishedYes

Fingerprint

Experimental Arthritis
T-Cell Antigen Receptor
Interferons
Arthritis
Collagen
Joints
Inbred DBA Mouse
Bearings (structural)
Interferon Receptors
T-cells
Collagen Type II
Freund's Adjuvant
Joint Diseases
Disease Susceptibility
Major Histocompatibility Complex
Interleukin-1
Inbred C57BL Mouse
Autoantibodies
Tumor Necrosis Factor-alpha
Immunoglobulin G

ASJC Scopus subject areas

  • Rheumatology
  • Immunology

Cite this

IFNγ deficient C57BL/6 (H-2b) mice develop collagen induced arthritis with predominant usage of T cell receptor Vβ6 and Vβ8 in arthritic joints. / Chu, Cong-Qiu; Song, Z.; Mayton, L.; Wu, B.; Wooley, P. H.

In: Annals of the Rheumatic Diseases, Vol. 62, No. 10, 01.10.2003, p. 983-990.

Research output: Contribution to journalArticle

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abstract = "Background: Transgenic deficiency in interferon γ (IFNγ) or IFNγ receptor makes resistant strains of mice bearing H-2b or H-2d susceptible to collagen induced arthritis (CIA). Objective: To determine whether the escape from regulation of disease susceptibility at the major histocompatibility complex level involves a new use of autoimmune T cells expressing T cell receptor (TCR) Vβ that vary from the cell populations previously identified within arthritic joints. Methods: Arthritis was induced by a standard protocol with type II bovine collagen (CII) in complete Freund's adjuvant. Clinical features, histopathology, immunological responses, and TCR profile in arthritic joints in IFNγ knockout C57BL/6 (B6.IFNγ KO) mice (H-2b) were compared directly with those in DBA/1 mice (H-2 q). Results: 60-80{\%} of B6.IFNγ KO mice developed a progressive arthritis with a similar clinical course to classical CIA in DBA/1 mice. The affected joints in B6.IFNγ KO mice had an erosive form of arthritis with similar features to joint disease in DBA/1 mice. B6.IFNγ KO mice produced significantly higher levels of IgG2b and IgG1 autoantibodies to murine CII and showed increased proliferative response to CII compared with B6 mice. Comparable levels of interleukin 1β and tumour necrosis factor α expression were detected in arthritic joints from B6.IFNγ KO and DBA/1 mice. B6.IFNγKO mice used predominantly TCR Vβ6 and Vβ8 in arthritic joints. This TCR Vβ profile is similar to that found in DBA/1 mice with CIA. Conclusions: C57BL/6 mice deficient in IFNγ production can develop arthritis that resembles classical CIA. These data suggest that IFNγ is a key factor mediating susceptibility to CIA.",
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AU - Wu, B.

AU - Wooley, P. H.

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N2 - Background: Transgenic deficiency in interferon γ (IFNγ) or IFNγ receptor makes resistant strains of mice bearing H-2b or H-2d susceptible to collagen induced arthritis (CIA). Objective: To determine whether the escape from regulation of disease susceptibility at the major histocompatibility complex level involves a new use of autoimmune T cells expressing T cell receptor (TCR) Vβ that vary from the cell populations previously identified within arthritic joints. Methods: Arthritis was induced by a standard protocol with type II bovine collagen (CII) in complete Freund's adjuvant. Clinical features, histopathology, immunological responses, and TCR profile in arthritic joints in IFNγ knockout C57BL/6 (B6.IFNγ KO) mice (H-2b) were compared directly with those in DBA/1 mice (H-2 q). Results: 60-80% of B6.IFNγ KO mice developed a progressive arthritis with a similar clinical course to classical CIA in DBA/1 mice. The affected joints in B6.IFNγ KO mice had an erosive form of arthritis with similar features to joint disease in DBA/1 mice. B6.IFNγ KO mice produced significantly higher levels of IgG2b and IgG1 autoantibodies to murine CII and showed increased proliferative response to CII compared with B6 mice. Comparable levels of interleukin 1β and tumour necrosis factor α expression were detected in arthritic joints from B6.IFNγ KO and DBA/1 mice. B6.IFNγKO mice used predominantly TCR Vβ6 and Vβ8 in arthritic joints. This TCR Vβ profile is similar to that found in DBA/1 mice with CIA. Conclusions: C57BL/6 mice deficient in IFNγ production can develop arthritis that resembles classical CIA. These data suggest that IFNγ is a key factor mediating susceptibility to CIA.

AB - Background: Transgenic deficiency in interferon γ (IFNγ) or IFNγ receptor makes resistant strains of mice bearing H-2b or H-2d susceptible to collagen induced arthritis (CIA). Objective: To determine whether the escape from regulation of disease susceptibility at the major histocompatibility complex level involves a new use of autoimmune T cells expressing T cell receptor (TCR) Vβ that vary from the cell populations previously identified within arthritic joints. Methods: Arthritis was induced by a standard protocol with type II bovine collagen (CII) in complete Freund's adjuvant. Clinical features, histopathology, immunological responses, and TCR profile in arthritic joints in IFNγ knockout C57BL/6 (B6.IFNγ KO) mice (H-2b) were compared directly with those in DBA/1 mice (H-2 q). Results: 60-80% of B6.IFNγ KO mice developed a progressive arthritis with a similar clinical course to classical CIA in DBA/1 mice. The affected joints in B6.IFNγ KO mice had an erosive form of arthritis with similar features to joint disease in DBA/1 mice. B6.IFNγ KO mice produced significantly higher levels of IgG2b and IgG1 autoantibodies to murine CII and showed increased proliferative response to CII compared with B6 mice. Comparable levels of interleukin 1β and tumour necrosis factor α expression were detected in arthritic joints from B6.IFNγ KO and DBA/1 mice. B6.IFNγKO mice used predominantly TCR Vβ6 and Vβ8 in arthritic joints. This TCR Vβ profile is similar to that found in DBA/1 mice with CIA. Conclusions: C57BL/6 mice deficient in IFNγ production can develop arthritis that resembles classical CIA. These data suggest that IFNγ is a key factor mediating susceptibility to CIA.

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