Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.

TNF-Induced Adipose-Related Protein (TIARP) Regulates Autoimmune Arthritis Via the Suppression of IL-6.

Inoue1,  Asuka, Matsumoto2,  Isao, Tanaka-Watanabe2,  Yoko, Yamamoto2,  Kayo, Umeda2,  Naoto, Tanaka2,  Yuki, Sumida3,  Takayuki

Division of Clinical Immunology, Doctoral Program in Clinical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba/ JSPS Research Fellow, Tsukuba City, Ibaraki, Japan
University of Tsukuba
University of Tsukuba/ Inst Clin Med, Tsukuba City, Japan

Background and Objective:

Recently, we found that TNFa-induced adipose-related protein (TIARP) is dominantly expressed in spleens and joints in TNFa-dependent model such as glucose-292-phosphate isomerase (GPI)-induced arthritis. TIARP is a six-transmembrane protein induced by TNFa, interleukin-6 (IL-6) and IL-1b in adipose tissue, although mechanisms in the pathogenesis of arthritis remains unclear. To elucidate the role of TIARP in the development and pathogenesis of autoimmune arthritis, we have generated TIARP-deficient (TIARP-/-) mice.


(1) Collagen induced arthritis (CIA) was induced by immunization with 200mg of chicken typeII collagen (CII) emulsified in complete freund's adjuvant (CFA) to C57BL/6(B6) mice, followed by boost immunization after 21 days of primary immunization. The TIARP mRNA in spleens and joints was evaluated in CIA mice on day 14, 23, 28, by quantitative RT-PCR.

(2) We generated TIARP-/- in B6 background. TIARP-/- and wild type (WT) mice were immunized with CII as described methods above. The severity of arthritis was monitored by clinical score and evaluated histologically on day 60.

(3) The level of anti-CII antibodies (Abs) in serum were assessed by enzyme-linked immunosorbent assay (ELISA).

(4) Draining lymph nodes and splenocytes on day10 were cultured for 96hr with CII in vitro. IFNg, IL-17 and IL-4 in their culture supernatant were measured by ELISA.

(5) The level of IL-6 and TNFa in serum on day60 after CII immunization were measured by ELISA.


(1) In CIA model, the expression of TIARP mRNA in splenocytes was the highest in the early phase of arthritis (on day23). On the other hand, the expression in joints was accompanied with the joint swelling (on day28).

(2) The arthritis score in TIARP-/- mice was higher than that in WT mice. Histological analyses showed that a lot of neutrophil infiltration, synovial proliferation, and cartilage destruction.

(3) The level of anti-CII Abs in serum were not significantly different between TIARP-/- and WT mice.

(4) The amount of IFNg, IL-17 and IL-4 was not significantly different between TIARP-/- and WT mice.

(5) The serum IL-6 was significantly increased in TIARP-/- mice, whereas serum TNFa was not detected.


These findings suggest that TIARP might be a negative regulator against autoimmune arthritis via the suppression of IL-6. TIARP might be a future target for the treatment of rheumatoid arthritis.

To cite this abstract, please use the following information:
Inoue, Asuka, Matsumoto, Isao, Tanaka-Watanabe, Yoko, Yamamoto, Kayo, Umeda, Naoto, Tanaka, Yuki, et al; TNF-Induced Adipose-Related Protein (TIARP) Regulates Autoimmune Arthritis Via the Suppression of IL-6. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :292
DOI: 10.1002/art.28061

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