CD1b is an MHC class I-like antigen-presenting glycoprotein that presents lipid and glycolipid antigens to T-cell receptors on αβ T cells and natural killer T cells 1. CD1b possesses the largest and most complex antigen-binding groove among CD1 family members, enabling presentation of a broad spectrum of self and foreign lipid antigens 2. The CD1b binding cleft exhibits a distinctive size mismatch with its ligands, accommodating two small lipids simultaneously within one cleft 3. CD1b presents both endogenous self-lipids—particularly phosphatidylglycerol and diacylglycerols—and exogenous bacterial lipids from pathogens including Mycobacterium tuberculosis and Borrelia burgdorferi 1, 4, 5. CD1b-restricted T cell responses recognize both self and foreign lipid antigens with notable cross-reactivity, suggesting a dual immune surveillance mechanism for detecting infection or stress-associated lipids 1, 4. During mycobacterial infection, CD1b expression is transiently upregulated at the transcriptional level during the effector phase of adaptive immunity, correlating with cytotoxic CD1b-restricted T cell activity in pulmonary granulomas 5. CD1b expression is downregulated in atopic dermatitis skin lesions and reduced by anti-IL-4 receptor therapy, implicating CD1b in TH2-mediated inflammatory diseases 6.