CXCL10, also known as interferon-gamma-inducible protein 10 (IP-10), is a 10 kDa chemokine that binds to the receptor CXCR3. It regulates immune responses by activating and recruiting leukocytes like T cells, eosinophils, and monocytes, and is categorized as a Th1-chemokine [3]. The CXCL10-CXCR3 signaling pathway is involved in multiple biological processes, including T cell tumor infiltration, pain pathogenesis, and immune responses during viral infections.

In a mouse model of vitiligo, mice lacking Cxcl10 or treated with CXCL10-neutralizing antibody, as well as those that received Cxcr3(-/-) T cells, developed minimal depigmentation. This indicates that CXCL10 is critical for the progression and maintenance of depigmentation in vitiligo [2]. In a model of neuropathic pain, SNL-induced mechanical allodynia and heat hyperalgesia were attenuated by intra-DRG injection of Cxcr3 shRNA, and CXCL10 increased the number of action potentials in DRG neurons through CXCR3-mediated activation of p38 and ERK [1].

In conclusion, CXCL10 plays essential roles in various biological processes and disease conditions. Model-based research, especially the use of KO mouse models in vitiligo and neuropathic pain studies, has revealed its critical functions in disease progression. Understanding CXCL10 can potentially lead to new targeted treatment strategies for related diseases.

References:

1. Kong, Yan-Fang, Sha, Wei-Lin, Wu, Xiao-Bo, Ma, Ling-Jie, Gao, Yong-Jing. 2020. CXCL10/CXCR3 Signaling in the DRG Exacerbates Neuropathic Pain in Mice. In Neuroscience bulletin, 37, 339-352. doi:10.1007/s12264-020-00608-1. https://pubmed.ncbi.nlm.nih.gov/33196963/

2. Rashighi, Mehdi, Agarwal, Priti, Richmond, Jillian M, Luster, Andrew D, Harris, John E. . CXCL10 is critical for the progression and maintenance of depigmentation in a mouse model of vitiligo. In Science translational medicine, 6, 223ra23. doi:10.1126/scitranslmed.3007811. https://pubmed.ncbi.nlm.nih.gov/24523323/

3. Lee, Eun Young, Lee, Zang-Hee, Song, Yeong Wook. 2008. CXCL10 and autoimmune diseases. In Autoimmunity reviews, 8, 379-83. doi:10.1016/j.autrev.2008.12.002. https://pubmed.ncbi.nlm.nih.gov/19105984/