IL-6 blockade preferentially inhibits Th17 differentiation in collagen-induced arthritis

Related Experiment Video

Updated: Jun 10, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
12:59

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

Hiroto Yoshida1, Misato Hashizume, Masahiko Mihara

  • 1Product Research Department, Fuji-Gotemba Research Laboratories, Chugai Pharmaceutical Co., Ltd., 1-135, Komakado, Gotemba, Shizuoka 412-8513, Japan.

Rheumatology International
|July 27, 2010
PubMed

We examined the time course of cytokine production by CD4 T cells from mice with collagen-induced arthritis (CIA), and we determined the influence of interleukin-6 (IL-6) blockade on cytokine production. CD4 T cells purified from spleen were cultured with both collagen and anti-CD28 antibody for 48 h and the production of interferon-γ (IFN-γ), IL-4, and IL-17 by the cells, secreted into the supernatants, was measured at various time intervals. The production of all these cytokines started 7 days after the first immunization. A marked increase in IFN-γ production was observed after the second immunization, but IL-4 and IL-17 production was not affected by a second immunization. A single injection of anti-mouse IL-6 receptor antibody (MR16-1) on the day of the first immunization suppressed the onset of arthritis. IL-17 production by CD4 T cells from MR16-1-treated mice was significantly lower than that from the control mice. On the other hand, treatment with MR16-1 showed only a tendency to suppress the production of IL-4 and IFN-γ. Injection of MR16-1 on day 21 did not suppress the onset of arthritis. We examined the direct influence of MR16-1 on cytokine production by differentiated CD4 T cells from arthritic mice. Production of IL-4, IFN-γ, and IL-17 was not affected by MR16-1. In conclusion, IL-6 inhibition preferentially suppresses the induction of Th17 cells and does not seem to impact on cytokine production of already differentiated Th17 cells.

More Related Videos

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase (G6PI)-Induced RA Mice08:43

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase (G6PI)-Induced RA Mice

Published on: January 31, 2020

In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse07:46

In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse

Published on: October 25, 2024

Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

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...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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...
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

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 Disease...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

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 (Humira),...