IL-23 Antibody Development Service

Interleukin-23 (IL-23) antibodies have become one of the research projects fucus on controlling the inflammatory response in the development of autoimmune diseases. Our company provides leading research services to assist you to develop antibodies with high specificity and expedite the therapeutic antibodies development in Autoimmune Diseases & Inflammation.

IL-23 in Autoimmune Diseases & Inflammation

IL-23 is one of the central members promoting inflammation in a broad range of autoimmune diseases. As an upstream factor, IL-23 induces the generation of IL-17 and IL-22 to regulate differentiation of T cells into Th17 cells, further facilitating the proliferation of IL-17-expressing T cells. Meanwhile, IL-23 stabilizes the transcription profile of Th17 through a STAT3-dependent pathway that is also shared with IL-6. Uncontrolled IL-23 stimulates the ectopic expression of IL-17, which continues to activate the production of more cytokines, thus creating a vicious cycle that leads to chronic inflammation in autoimmune diseases.

Fig.1 The pathophysiology model of immune-mediated inflammatory diseases centered on IL-23  (Bunte K., et al., 2019)

• IL-23 in Rheumatiod Arthritis
  The activation of macrophages located in synovial tissue evokes the release of IL-23 and other pro-inflammatory cytokines to initiate the differentiation of Th17 cells, followed by the IL-17 stimulating the production of a group of cytokines, and disrupting the remodeling and formation of bones directly or indirectly. In turn, IL-17 in combination with TNFα continues to stimulate IL-23 production, forming a detrimental feedback loop that promotes inflammation.

• IL-23 in Inflammatory Bowel Disease
  Activate T cells secret IL-23, which induce the generation of plenty cytokines, including TNFα, IL-6, IL-1, to promote inflammation through the formation and differentiation of Th17 cells. Then IL-17 from Th17 cells and γδT cells induces cytokines and chemokines, comprising IL-6, CXCLs and MMPs. Furthermore, IL-23 induces accumulation of CD11b+ dendritic cells at sites of inflammatory bowel diseases, causing the tissue injuries jointly.

• IL-23 in Idiopathic Pulmonary Fibrosis
  A significant increase of the level of IL-23 is observed in the serum of patients with Idiopathic pulmonary fibrosis (IPF), and the expression of IL-22 and IL-17 from CD4+ T cells also elevated by the induction of IL-23. Combined with IL-6 and TGFβ, IL-23 involves in the formation and differentiation of Th17 cells. Moreover, the IL-23 positive CD11B+ cells are increased in the fibrotic lung, leading to the release of keratinocyte derived cytokines in the bronchoalveolar, which recruit lymphocytes and neutrophils to promote the exacerbation of emphysema.

A variety of cytokines and signaling pathways form an intricate regulatory relationship with IL-23 in the autoimmune response. The mechanism of IL-23 is yet to be fully understood, however, this does not diminish its central role in the inflammatory response, thus necessitating the development of therapeutic antibodies.

Our Services

IL-23 and the members of its pathways giving rise to continuous inflammation in Autoimmune Diseases & Inflammation have attracted a lot of attention for developing promising therapeutic antibodies. Our company provides comprehensive coordinated-process of antibodies development services for IL-23 signaling pathways as the following workflow: 

Antigen Validation

IL-23 signaling pathways

Antibody Generation

Antibody Optimization

Antibody Characterization

Antibody Production & Purification

Our advantages

With cutting-edge cellular immunology equipment and personnel with extensive experience in antibody development, our company is devoted to providing quality services for the development of therapeutic antibodies to IL-23 signaling pathways. If you are interested in our services, please contact us for more detailed information.

Reference

1. Bunte, Kübra, and Thomas Beikler. "Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases." International journal of molecular sciences 20,14 (2019): 3394.