Ticam1, also known as Toll-like receptor adaptor molecule 1, is a key coding gene involved in immune and inflammation responses to malignant cells. It is an essential adaptor protein in Toll-like receptor (TLR) signaling pathways, especially in the TLR3-and TLR4-mediated MyD88-independent pathway. TLRs play a crucial role in activating innate immunity by recognizing microbial components, and Ticam1 contributes to the specificity of TLR signaling [2].

In Wilms tumor (WT), Ticam1 was found to be downregulated in patients with worse prognosis and more advanced clinical stages. Low expression of Ticam1 led to less immune cell infiltration, fewer protective immune cells, and more antitumor immune cells, indicating its significant impact on the prognosis, progression, and immune infiltration of WT [1]. In children, Ticam1 gene polymorphisms were associated with community-acquired pneumonia (CAP). For example, the CC genotype of rs11466711T/C locus reduced the risk of childhood CAP, while certain genotypes and haplotypes were related to CRP level and sepsis in childhood CAP [3].

In conclusion, Ticam1 is vital in immune-related signaling pathways. Its role in diseases like Wilms tumor and childhood CAP is significant, as demonstrated through studies on gene expression levels and polymorphisms. These findings contribute to our understanding of disease mechanisms and may potentially offer new insights for diagnosis and treatment in these disease areas.

References:

1. Lu, Zhiyi, Sun, Fengyin. 2022. Downregulated TICAM1 is a prognostic biomarker and associated with immune tolerance of Wilms tumor patients. In BMC medical genomics, 15, 174. doi:10.1186/s12920-022-01326-5. https://pubmed.ncbi.nlm.nih.gov/35933370/

2. Takeda, Kiyoshi, Akira, Shizuo. . TLR signaling pathways. In Seminars in immunology, 16, 3-9. doi:. https://pubmed.ncbi.nlm.nih.gov/14751757/

3. Yang, Yong, Yang, Suiyu, Chen, Zongbo, Liu, Li. 2020. Correlation between TICAM1 gene polymorphisms and community-acquired pneumonia in children. In Journal of biochemical and molecular toxicology, 34, e22503. doi:10.1002/jbt.22503. https://pubmed.ncbi.nlm.nih.gov/32243044/