The Type I Interferon (IFN) Receptor has 2 subunits designated as IFNAR1 and IFNAR2. The IFNAR2 subunit is responsible for IFN binding while IFNAR1 confers high affinity to the receptor. We developed monoclonal antibodies (mAbs) that recognize both subunits of the human Type I Interferon Receptor (IFNAR). The anti-Type I Interferon Receptor monoclonal antibody IFNAR2, originally designated as IFNaRß1, recognizes the IFNAR2 subunit or binding subunit of the receptor. This mAb blocks binding of all alpha subtypes, beta, and omega IFNs to the receptor (Colamonici, O.R. et al. 1993, J. Biol. Chem. 268: 10895.)

The anti-IFNAR1 subunit of the Type I IFN receptor monoclonal antibody, was originally designated IFNaR3 mAb (Colamonici OR, et al. 1990, PNAS. 87:7230.) The mouse anti-IFNAR1 and anti-IFNAR2 mAbs can be directly purchased from PBL.

Humanized IFNAR2 Monoclonal Antibody

Type I IFNs play a role in autoimmune diseases such Systemic Lupus Erythematosus (SLE). We have recently humanized the IFNAR2 mAb to explore its potential treatment for autoimmune diseases in which Type I IFNs play a prominent role. The humanized IFNAR2 mAb binds to the IFNAR2 subunit of the Type I IFN-R with almost identical affinity as the original mouse mAb. Therefore, it could represent a valuable therapeutic tool for the treatment of specific autoimmune diseases. The humanized IFNAR2 monoclonal antibody is currently being tested in preclinical studies.