AI Article Synopsis
- Hydroxychloroquine (HCQ) is known for its anti-inflammatory properties, and this study evaluates its impact on anti-PD1 immunotherapy in various tumor models (MC38, CT26, RIL-175).
- The findings indicate that HCQ directly reduces tumor cell growth and negatively affects T-cell production of key cytokines like TNFα and IFNγ, which are important for immune response.
- HCQ treatment leads to a diminished response to anti-PD1 therapy by impairing T-cell activation and reducing the presence of CD8 T cells that target the tumor, suggesting that HCQ can hinder the effectiveness of this immunotherapy.
Article Abstract
Hydroxychloroquine (HCQ) is a well-known anti-inflammatory drug but is also known as an anti-inflammatory drug. Here, we evaluate the influence of HCQ treatment on the effect of anti-PD1 tumor immunotherapy. Anti-PD1 therapy-sensitive tumor lines MC38, CT26, and RIL-175 were used to investigate the impact of HCQ on anti-PD1 therapy efficacy. assays demonstrated that HCQ directly inhibited tumor cell growth in all the tested tumor cell lines. HCQ treatment impaired both antigen-specific and nonspecific T-cell production of TNFα and IFNγ and . Importantly, in all the three tumor models, HCQ treatment significantly impaired the response to anti-PD1 treatment, accompanying diminished T-cell activation and reduced tumor-infiltrating, antigen-specific CD8 T cells. This study shows that HCQ treatment can result in immunotherapy failure due to its immunosuppressive effects that offset both increased MHC-I expression by tumor cell and direct cytotoxicity.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7807148 | PMC |
| http://dx.doi.org/10.1016/j.isci.2020.101990 | DOI Listing |
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