IFN-I Antibody Development Service

Type I Interferons (IFN-I) antibodies have been applied to restrain the excessive IFN responses to prevent tissue damages from the overactive immune system. Our company provides leading research services to assist you to develop antibodies with high potency and to escort the development of therapeutic antibodies for Autoimmune Diseases & Inflammation.

IFN-I in Autoimmune Diseases & Inflammation

The IFN-I family contains 16 members, of which the most studied are multiple isoforms of IFN-α and IFN-β. The former is predominantly generated by plasmacytoid dendritic cells (pDCs), and the latter is produced by macrophages. When these cells are stimulated by the deposition of various autoimmune complexes, such as GM-CSF and IL-3 from activated T cells and PECAM-1 from B cells, type I INFs are expressed to trigger a chain of signals through JAK1-STAT, MAPK-ERK, PI3K-AKT-p38 or mTOR pathways to initiate the transcription of IFN stimulated genes (ISGs). Abnormal activation of these sophisticated networks is extensively detected in the inflammatory tissues of autoimmune diseases.

Fig.1 Type I interferons and immune complex formation contributes to organ damage in the cycle of systemic lupus erythematosus (SLE) pathophysiology. (Ramaswamy M., et al., 2021) 

• IFN-I in Systemic Lupus Erythematosuss

Heightened levels of IFN-1 and IFN-1-regulated genes are typical phenotype of SLE. The autoantigens released by apoptotic cells and neutrophil extracellular traps (NETs) from granulocytes trigger autoantibodies from B cells to form autoimmune complexes, which are endocytosed into the endosome of pDCs and activate IFN-α generation.

• IFN-I in Type 1 Diabetes

In type 1 diabetes, pDCs and islet β cells release excessive amounts of IFN-α into the blood. The INF-α overstocked in β cells induces endoplasmic reticulum stress, leading to the apoptosis and breakdown. Sustained IFN-β play a negative role to impair the expression of genes regulated by IL-10 signaling through the JAK-STAT pathway in T cells. Thus excessive IFN-α/β weaken the normal function of β cells.

• IFN-I in Sjögren's Syndrome

In exocrine epithelial cells, the IFN regulatory factors (IRF5 and IRF7) activated by stimuli from extra- or intra-cells promote the expression of IFN-I genes and other pro-inflammatory cytokines. High levels of IFN-I activate the TYK2 and JAK1 pathways to accelerate the transcription of ISGs, including IRF7, which in turn continues to stimulate IFN-I expression to form a pernicious feedback loop.

Multiple cell types and signaling pathways participate in the complex network regulated by IFN-I in the autoimmune response. Both genetic and epigenetic factors can exert their effects on IFN-I signaling pathway, which makes the intervention of various targets in the IFN-I signaling pathways using therapeutic antibodies a hope to suppress inflammation.

Our Services

Several blocking therapies targeting IFN-I signaling pathways in Autoimmune Diseases & Inflammation have attracted much attention. Our company provides comprehensive coordinated-process of antibodies development services for IFN-I signaling pathways as the following workflow: 

Antigen Validation

IFN-I signaling pathways

Antibody Generation

Antibody Optimization

Antibody Characterization

Antibody Production & Purification

Our advantages

With the participation of high-level experts in antibody science and other disciplines, as well as the top antibody preparation line, our company is devoted to providing quality services for the development of therapeutic antibodies to IFN-I signaling pathways. If you are interested in our services, please contact us for more detailed information.

Reference

1. Ramaswamy, Madhu et al. "The Pathogenesis, Molecular Mechanisms, and Therapeutic Potential of the Interferon Pathway in Systemic Lupus Erythematosus and Other Autoimmune Diseases." International journal of molecular sciences 22,20 (2021): 11286.