Related Experiment Video
Updated: Apr 3, 2026
07:37
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
1.4K
CTRP6 is an endogenous complement regulator that can effectively treat induced arthritis
Masanori A Murayama1,2,3,4, Shigeru Kakuta2, Asuka Inoue5
1Division of Experimental Animal Immunology, Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Chiba 278-0022, Japan.
Nature Communications
|September 26, 2015
Summary
C1q/TNF-related protein 6 (CTRP6) regulates the complement system, a key part of immune defense and inflammation. CTRP6 deficiency worsens arthritis, while CTRP6 treatment cures it, suggesting therapeutic potential for complement-mediated diseases.
Area of Science:
- Immunology
- Complement System Biology
- Rheumatology
Background:
- The complement system is crucial for host defense and inflammatory disease development.
- Rheumatoid arthritis (RA) involves complex immune dysregulation.
- Understanding novel regulators of complement activation is vital for therapeutic strategies.
Purpose of the Study:
- To investigate the role of C1q/TNF-related protein 6 (CTRP6) in arthritis and complement activation.
- To determine the mechanism by which CTRP6 modulates the complement system.
- To evaluate the therapeutic potential of CTRP6 in complement-mediated inflammatory conditions.
Main Methods:
- Utilized mouse models of rheumatoid arthritis and other inflammatory conditions (Arthus reaction, experimental autoimmune encephalomyelitis).
- Generated and analyzed C1qtnf6 knockout and transgenic mice.
- Investigated the molecular interaction of CTRP6 with complement components, specifically Factor B and C3(H2O).
- Administered recombinant human CTRP6 via intra-articular injection in disease models.
Main Results:
- CTRP6 expression is elevated in mouse rheumatoid arthritis models.
- C1qtnf6 knockout mice exhibit heightened susceptibility to arthritis due to increased complement activation.
- CTRP6 directly inhibits the alternative complement pathway by preventing Factor B binding to C3(H2O).
- Intra-articular CTRP6 administration effectively resolved arthritis in treated mice.
- CTRP6 is present in human synoviocytes and elevated in RA patients.
Conclusions:
- CTRP6 functions as an endogenous regulator of the complement system, primarily suppressing the alternative pathway.
- CTRP6 deficiency exacerbates inflammatory responses mediated by complement.
- CTRP6 demonstrates significant therapeutic efficacy in treating arthritis and holds promise for treating complement-mediated diseases.
Related Concept Videos
01:24Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
759
Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
759
01:24T Cell Types and Functions
3.3K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
3.3K
01:29Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents
684
Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
684