The role of IL-10 in animal models of viral infection has not been investigated extensively. Nevertheless, a study of Herpes Simplex Virus-1 (HSV-1) induced stromal keratitis in mice, characterized by ocular inflammation leading to blindness, demonstrated that intraperitoneal administration of IL-10 reduced the incidence of blindness, cellular infiltration and levels of IL-2 and IL-6 in the cornea. However, IL-10 did not influence virus clearance from the eye.46
Table 1. Summary of the role of IL-10 in disease outcome for various pathogens in experimental mouse models
Organism / Disease Model
Method of IL-10 Disease Status
Modulation Resistance (R)/Susceptibility (S) References
M. tuberculosis M. avium
Trypanosoma congolense Toxoplasma gondii Plasmodium yoelii Plasmodium chabaudi Viral Infections
Herpes Simplex Virus Vaccinia Virus JHMV EMCV Fungi
rIL-10 IL-10 Tg IL-10 KO Anti-IL-10 IL-10 KO Anti-IL-10 Anti-IL-10
rIL-10 Anti-IL-10 IL-10 Tg IL-10 KO IL-10 KO Anti-IL-10 Anti-IL-10 Anti-IL-10 IL-10 KO
rIL-10 Anti-IL-10 IL-10 KO IL-10
rIL-10 IL-10 Tg Anti-IL-10 IL-10 KO
rIL-10 Anti-IL-10 IL-10 KO Anti-IL-10 IL-10 KO IL-10 KO IL-10 KO
rIL-10 / plasmid IL-10 KO IL-10 KO rIL-10
rIL-10 Anti-IL-10 IL-10 KO IL-10 KO IL-10 KO Anti-IL-10 IL-10 KO
In another study of herpetic stromal keratitis, established ocular lesions could be controlled in the majority of animals by the administration of a plasmid DNA encoding IL-10.47 In a recent study on acute vaccinia virus infection, Van der Broek et al demonstrated that virus replication was impaired in IL-10 KO mice, which was associated with its impact on IL-12 expression and the induction of cytotoxic T lymphocyte (CTL) responses.48 Neurotropic mouse hepatitis virus (JHMV)-induced demyelinating encaphalomyelitis has also been investigated in IL-10 KO mice wherein increased morbidity and mortality were observed.49 This was associated with increased central nervous system (CNS) inflammation, and production of inflammatory mediators (TNF-a, IFN-y and iNOS), however, IL-10 was not required for elimination of infectious virus from the brain.49 In a murine model of viral myocarditis caused by encephalomyocarditis virus (EMCV), IL-10 administration reduced myocardial lesions resulting in enhanced survival compared to control animals but did not affect virus replication.50 Taken together, in the viral infections exhibiting inflammatory pathology, these observations suggest that although IL-10 is not required for viral clearance, it appears to be one of the mechanisms responsible for inhibiting the extent of inflammation.
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