Anti-IFNAR Recombinant Antibody (TAB-722) (CAT#: TAB-722)

Bender, Andrew T., et al. "TLR7 and TLR8 differentially activate the IRF and NF-κB pathways in specific cell types to promote inflammation." Immunohorizons 4.2 (2020): 93-107. https://doi.org/10.4049/immunohorizons.2000002

This study investigates how TLR7 and TLR8 differentially activate the IRF and NF-κB pathways in specific cell types to promote inflammation. TLR7 and TLR8 are endosomal receptors that recognize single-stranded RNA (ssRNA) and play critical roles in antiviral defense and the pathogenesis of autoimmune diseases such as lupus. The research uses cell sorting, gene expression analysis, and intracellular cytokine staining to characterize the effects of TLR7 and TLR8 activation in various human immune cells. The study found that TLR7 primarily activates the IRF pathway leading to type I IFN production, while TLR8 predominantly activates the NF-κB pathway, resulting in the production of inflammatory cytokines. These findings enhance the understanding of the distinct roles TLR7 and TLR8 play in immune responses and their contributions to autoimmune diseases.
Creative Biolabs provided the anti-IFNAR antibody anifrolumab (Cat#: TAB-722) used in this study. Anifrolumab was crucial in experiments designed to block type I IFN activity, allowing researchers to differentiate between gene expression changes directly induced by TLR7/8 activation and those mediated by secondary IFN responses. The antibody was pivotal in demonstrating that inhibiting IFN activity can prevent secondary IFN-induced gene expression while not affecting NF-κB-regulated genes directly induced by TLR7/8 activation. This contribution was essential for elucidating the distinct pathways and effects mediated by TLR7 and TLR8 activation in various cell types.

Zheng, Jian, et al. "Severe acute respiratory syndrome coronavirus 2-induced immune activation and death of monocyte-derived human macrophages and dendritic cells." The Journal of infectious diseases 223.5 (2021): 785-795. https://doi.org/10.1093/infdis/jiaa753

This study examines the infection and immune response of human monocyte-derived macrophages (MDMs) and dendritic cells (MDDCs) by SARS-CoV-2. The research found that although SARS-CoV-2 infects these cells abortively, it still induces the production of multiple proinflammatory cytokines and chemokines, such as IFN-α, IFN-β, TNF, IL-1β, IL-6, IL-8, IL-10, and CXCL10. This infection triggers a type I IFN-mediated cell death, contributing to the inflammatory response observed in COVID-19. The study also demonstrated that infection is dependent on the ACE2 receptor and that the presence of convalescent plasma can block this infection without enhancing macrophage cell death, suggesting the non-involvement of antibody-dependent enhancement in cell death.
Creative Biolabs provided the IFN-α receptor (IFNAR) monoclonal antibody Anifrolumab (Cat#: TAB-722) used to block type I IFN signaling in this study. The antibody was crucial in demonstrating that blocking IFNAR reduced the percentage of cell death in SARS-CoV-2-infected MDMs. This blocking assay helped to reveal the role of type I IFNs in mediating the apoptosis of MDMs post-infection, thereby offering insights into the mechanisms of macrophage activation and cell death during SARS-CoV-2 infection.

Gong, Ke, et al. "EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer." Nature cancer 1.4 (2020): 394-409. https://doi.org/10.1038/s43018-020-0048-0

This study explores the impact of EGFR inhibition on type I interferon (IFN) signaling in non-small cell lung cancer (NSCLC). Researchers found that inhibiting EGFR in NSCLC triggers an antiviral defense mechanism, resulting in the upregulation of type I IFNs via the RIG-I-TRIM32-TBK1-IRF3 pathway in EGFR-mutant cells, and via an NF-κB-dependent pathway in EGFR wild-type (EGFRwt) cells. The study demonstrates that the upregulation of type I IFNs contributes to both primary and secondary resistance to EGFR-tyrosine kinase inhibitors (TKIs). Additionally, the study suggests that combining EGFR-TKI treatment with IFN signaling inhibition could improve treatment efficacy and overcome resistance in both EGFR-mutant and EGFRwt NSCLC.
Creative Biolabs provided the anifrolumab antibody (Cat#: TAB-722) used in this study. Anifrolumab was crucial for experiments involving the inhibition of type I IFN signaling. The use of anifrolumab allowed researchers to demonstrate that blocking IFNAR enhances the sensitivity of NSCLC cells to EGFR inhibition, thereby reducing cell survival and preventing the development of resistance to EGFR-TKIs. This antibody was essential in illustrating the potential therapeutic benefit of combining EGFR-TKIs with IFN signaling inhibitors to improve treatment outcomes in NSCLC.