Related Experiment Video
Updated: Aug 3, 2025

06:38
Induction of Ocular Surface Inflammation and Collection of Involved Tissues
Published on: August 4, 2022
2.3K
IL-27 attenuates IL-23 mediated inflammatory arthritis
Ritu Sarin1, Ran Gu1, Zahra Jalali2
1Department of Internal Medicine, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis Medical Center, Sacramento, CA, USA.
Clinical Immunology (Orlando, Fla.)
|April 10, 2023
Summary
Interleukin 27 (IL-27) suppresses inflammation by reducing myeloid cell expansion in bone marrow and joints. This study reveals IL-27
Area of Science:
- Immunology
- Autoimmunity
- Inflammation Research
Background:
- Interleukin 27 (IL-27) exhibits dual roles in autoimmunity, with known anti-inflammatory effects on Th17 cells.
- The impact of IL-27 on myeloid cells in inflammatory conditions remains less understood.
Purpose of the Study:
- To investigate the role of IL-27 in regulating IL-23-induced inflammation, focusing on myeloid cell populations.
- To elucidate the immunosuppressive mechanisms of IL-27 in the context of inflammatory arthritis.
Main Methods:
- Analysis of myeloid cell infiltration in joints and spleens.
- Quantification of myeloid cell populations in spleen and bone marrow.
- Assessment of IL-27's effect on IL-23-driven inflammatory responses.
Main Results:
- IL-27 significantly inhibited IL-23-induced inflammation, reducing myeloid cell infiltration in joints.
- IL-27 decreased specific myeloid cell subsets (CD11b+ GR1+ and CD3-CD11b+CD11c-GR1-) in the spleen.
- Reduced myeloid cell levels were observed in the spleen and bone marrow following IL-27 treatment.
Conclusions:
- IL-27 demonstrates a significant immunosuppressive function by modulating IL-23-dependent myelopoiesis.
- IL-27 plays a critical role in controlling joint inflammation by negatively regulating myeloid cell expansion.
- These findings highlight IL-27 as a potential therapeutic target for inflammatory arthritis.
Related Concept Videos
T Cell Types and Functions
1.1K
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...
1.1K
The JAK-STAT Signaling Pathway
9.1K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
9.1K
Inflammatory Response
2.4K
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
2.4K
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
188
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...
188

