Fcnb, also known as ficolin-B, is a recognition molecule. It can recognize various ligands and is involved in mediating the cell cycle, immune response, and tissue homeostasis in the lung. Fcnb is associated with the cGAS-STING signaling pathway, and plays a role in innate immunity by potentially activating the complement system via the lectin pathway upon binding to certain patterns [1,4]. Mouse genetic models, such as Fcnb-/-mice, are valuable for studying its functions [1,2,3].

In the context of bleomycin-induced lung injury, macrophage-derived Fcnb transported by exosomes exacerbates the injury and fibrosis. It promotes autophagy and ferroptosis in lung epithelial cells through the activation of the cGAS-STING pathway. In contrast, inhibiting autophagy-dependent ferroptosis can reverse this effect [1]. In a sepsis-induced severe lung injury model, knockout of Fcnb does not alleviate the injury, indicating its non-protective role in this condition compared to Fcna knockout [3]. Also, recombinant Fcnb binds to late apoptotic cells, apoptotic bodies, and necrotic cells in a calcium-dependent manner, suggesting its role in the removal of damaged host cells [4]. LncRNA AK036396 can enhance Fcnb protein stability, which in turn inhibits the maturation and accelerates the immunosuppression of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) [5].

In conclusion, Fcnb is involved in multiple biological processes related to immune response and tissue homeostasis. The study of Fcnb using gene knockout mouse models has revealed its role in diseases such as lung injury and in processes like cell death and immune cell regulation. Understanding Fcnb can provide insights into the mechanisms of these diseases and potentially lead to new therapeutic strategies [1,3,4,5].

References:

1. Wu, Xu, Jiang, Yixia, Li, Rong, Li, Guoqing, Tan, Xiaowu. 2023. Ficolin B secreted by alveolar macrophage exosomes exacerbates bleomycin-induced lung injury via ferroptosis through the cGAS-STING signaling pathway. In Cell death & disease, 14, 577. doi:10.1038/s41419-023-06104-4. https://pubmed.ncbi.nlm.nih.gov/37648705/

2. Huang, Li, Tan, Xiaowu, Xuan, Weixia, Jiang, Yongliang, Wu, Xu. 2024. Ficolin-A/2 Aggravates Severe Lung Injury through Neutrophil Extracellular Traps Mediated by Gasdermin D-Induced Pyroptosis. In The American journal of pathology, 194, 989-1006. doi:10.1016/j.ajpath.2024.02.011. https://pubmed.ncbi.nlm.nih.gov/38442803/

3. Wu, Xu, Xuan, Weixia, Yang, Xiaoping, Cao, Bin, Jiang, Yongliang. 2023. Ficolin A knockout alleviates sepsis-induced severe lung injury in mice by restoring gut Akkermansia to inhibit S100A4/STAT3 pathway. In International immunopharmacology, 121, 110548. doi:10.1016/j.intimp.2023.110548. https://pubmed.ncbi.nlm.nih.gov/37356123/

4. Schmid, Maximilian, Hunold, Katja, Weber-Steffens, Dorothea, Männel, Daniela N. 2011. Ficolin-B marks apoptotic and necrotic cells. In Immunobiology, 217, 610-5. doi:10.1016/j.imbio.2011.10.020. https://pubmed.ncbi.nlm.nih.gov/22119501/

5. Tian, Xinyu, Zheng, Yu, Yin, Kai, Xu, Huaxi, Wang, Shengjun. 2020. LncRNA AK036396 Inhibits Maturation and Accelerates Immunosuppression of Polymorphonuclear Myeloid-Derived Suppressor Cells by Enhancing the Stability of Ficolin B. In Cancer immunology research, 8, 565-577. doi:10.1158/2326-6066.CIR-19-0595. https://pubmed.ncbi.nlm.nih.gov/32102837/