Ltb, related to leukotriene B4 (LTB4) which is a lipid mediator produced from arachidonic acid, plays a crucial role in inflammatory processes. LTB4 acts as a chemoattractant for inflammatory leukocytes, and is involved in the leukocyte recruitment, pathogen elimination, and various inflammatory diseases through its receptors BLT1 and BLT2 [2]. It also participates in a cascade with complement, lipid, cytokine and chemokine to initiate and sustain neutrophilic inflammation in inflammatory arthritis [1].

Genetic models have been instrumental in understanding Ltb's functions. For example, in BLT1 -deficient mice, the LTB4/BLT1 axis was found to enhance leukocyte recruitment to infected sites, highlighting its role in host defense [2]. In a study of chronic granulomatous disease, antagonizing BLT1 blocked neutrophil aggregation in an ex vivo pyogranuloma formation system using peritoneal cells of CGD (gp91phox -/-) mice, suggesting LTB4's key role in pyogranuloma formation [4]. Also, in Lta4h -/- mice, blocking the LTB4 signaling enhanced the efficacy of immunotherapy against lung cancer, indicating LTB4 signaling's involvement in tumor - associated macrophages (TAMs) recruitment and immunosuppression [3].

In conclusion, Ltb, through its association with LTB4, is essential in inflammatory responses, host defense, and disease - related processes such as in inflammatory arthritis, chronic granulomatous disease, and lung cancer. Studies using gene - knockout mouse models have significantly contributed to revealing its roles in these disease areas, providing insights into potential therapeutic targets.