Interferon-induced transmembrane protein 10 (IFITM10) is a highly conserved member of the IFITM protein family . The IFITM family is known for its antiviral properties, preventing viral infection early in the viral lifecycle . IFITM10 exists in aquatic and terrestrial forms, indicating that it may be associated with adaptation to different environments .
A study identified 174 IFITM orthologous genes and 112 pseudogenes from 27 vertebrate genome sequences, dividing the vertebrate IFITM family into sub-families .
IP-10 mRNA expression can be induced in vitro and in vivo in glomerular and tubulointerstitial cells, suggesting its involvement in renal damage modulation in experimental nephrosis .
IFITM10 expression is positively correlated with the expression levels of CD69, CD44, NKp30, and granzyme B, which are important for immune cell function . In patients recovering from COVID-19, IFITM10 expression levels are substantially higher than in patients with persistent viral shedding .
IFITM10 expression is negatively correlated with ID1 expression, which is implicated in immune suppression .
IFITM proteins, including IFITM10, have demonstrated the ability to prevent viral infections during the early stages of viral lifecycles .
Various compounds and conditions can affect IFITM10 expression :
Increased expression: Copper, Diquat, Esketamine, Hydrogen Peroxide, Ketamine, Oxygen deficiency co-treated with Blood Glucose deficiency co-treated with Particulate Matter
Decreased expression: DDE (Dichlorodiphenyl Dichloroethylene), Diisodecyl phthalate, Doxorubicin
In chickens, IFITM10 levels are significantly lower than IFITM3, an antiviral protein .
IP-10-deficient mice exhibit impaired T cell responses, characterized by decreased proliferation, reduced IFN-γ secretion, and impaired contact hypersensitivity responses .
Mice lacking IP-10 show an impaired ability to control viral replication in the brain, which is associated with decreased recruitment of CD4+ and CD8+ lymphocytes, reduced levels of IFN-γ, and impaired generation of viral-specific CD8+ T cells .