CD121b, also known as interleukin-1 receptor type 2 (IL1R2), is a member of the interleukin-1 receptor family. It was first identified in the early 1990s as a decoy receptor that modulates the activity of IL-1. a key pro-inflammatory cytokine. Unlike the signaling receptor IL1R1. CD121b lacks a Toll/IL-1 receptor (TIR) domain, rendering it incapable of initiating intracellular signaling. Instead, it binds IL-1β and IL-1α with high affinity, sequestering them to inhibit their interaction with IL1R1 and downstream inflammatory pathways. This regulatory mechanism is critical in balancing immune responses and preventing excessive inflammation.
CD121b is expressed on immune cells, including B cells, monocytes, and neutrophils, as well as non-immune cells like fibroblasts. Its expression can be upregulated by anti-inflammatory mediators such as IL-4 and glucocorticoids, highlighting its role in immune homeostasis. Dysregulation of CD121b has been implicated in chronic inflammatory diseases, autoimmune disorders, and cancer, where altered IL-1 signaling contributes to pathogenesis.
Antibodies targeting CD121b are valuable tools for studying IL-1 signaling dynamics, detecting receptor expression in tissues, or developing therapeutic strategies to modulate inflammation. For example, CD121b-specific antibodies may enhance IL-1 neutralization in diseases driven by IL-1 overactivity, such as rheumatoid arthritis. Research continues to explore its therapeutic potential and mechanistic nuances in immune regulation.