C57BL/6JCya-Nlrp10^em1/Cya

Nlrp10, a NOD-like receptor, lacks a canonical leucine-rich repeat domain. It functions in multiple immune-related pathways. Nlrp10 is involved in inflammasome formation, regulation of inflammatory responses, and maintenance of tissue homeostasis. It can interact with proteins like Abin-1 to control inflammatory signaling, and is associated with pathways such as NF-κB activation [3]. Genetic models, like KO mouse models, have been crucial in studying its functions.

In KO mouse models, whole-body or conditional IEC Nlrp10 depletion led to reduced IEC caspase-1 activation and enhanced susceptibility to dextran sodium sulfate-induced colitis, indicating its role in protecting against intestinal autoinflammation [1]. NLRP10 ablation in mice protected against ischemia/reperfusion-associated brain injury by suppressing neuroinflammation, as it decreased infarct volume, improved movement, alleviated apoptosis, and inhibited glia cell activation and inflammatory factor levels [2]. In Nlrp10 -/- mice, there was diminished T helper 1-cell responses and increased bacterial growth upon Mycobacterium tuberculosis infection, showing its importance in promoting host defense [4]. Also, Nlrp10 -/- mice had reduced inflammation in DNFB-induced contact hypersensitivity response, highlighting its role in T-cell-mediated skin inflammatory responses [5].

In conclusion, Nlrp10 plays essential roles in innate and adaptive immunity, tissue homeostasis, and protection against various inflammatory conditions. Studies using KO mouse models have revealed its significance in intestinal autoinflammation, ischemic stroke, host defense against tuberculosis, and skin inflammatory responses, providing insights into potential therapeutic targets for related diseases.

References:

1. Zheng, Danping, Mohapatra, Gayatree, Kern, Lara, Abdeen, Suhaib K, Elinav, Eran. 2023. Epithelial Nlrp10 inflammasome mediates protection against intestinal autoinflammation. In Nature immunology, 24, 585-594. doi:10.1038/s41590-023-01450-z. https://pubmed.ncbi.nlm.nih.gov/36941399/

2. Li, Zhi-Guo, Shui, Shao-Feng, Han, Xin-Wei, Yan, Lei. 2020. NLRP10 ablation protects against ischemia/reperfusion-associated brain injury by suppression of neuroinflammation. In Experimental cell research, 389, 111912. doi:10.1016/j.yexcr.2020.111912. https://pubmed.ncbi.nlm.nih.gov/32084391/

3. Mirza, Nora, Sowa, Anna S, Lautz, Katja, Kufer, Thomas A. 2018. NLRP10 Affects the Stability of Abin-1 To Control Inflammatory Responses. In Journal of immunology (Baltimore, Md. : 1950), 202, 218-227. doi:10.4049/jimmunol.1800334. https://pubmed.ncbi.nlm.nih.gov/30510071/

4. Vacca, Maurizio, Böhme, Julia, Zambetti, Lia Paola, Singhal, Amit, Mortellaro, Alessandra. 2017. NLRP10 Enhances CD4+ T-Cell-Mediated IFNγ Response via Regulation of Dendritic Cell-Derived IL-12 Release. In Frontiers in immunology, 8, 1462. doi:10.3389/fimmu.2017.01462. https://pubmed.ncbi.nlm.nih.gov/29163529/

5. Damm, Anna, Giebeler, Nives, Zamek, Jan, Zigrino, Paola, Kufer, Thomas A. 2016. Epidermal NLRP10 contributes to contact hypersensitivity responses in mice. In European journal of immunology, 46, 1959-69. doi:10.1002/eji.201646401. https://pubmed.ncbi.nlm.nih.gov/27221772/