Immune Checkpoints as the Immune System Regulators and Potential Biomarkers in HIV-1 Infection
AbstractImmune checkpoints are several co-stimulatory and inhibitory pathways that regulate T cell immune responses. Most of the discoveries about immune checkpoints were made in cancer research where inhibitory immune checkpoints cause immune exhaustion and down-regulate anti-tumor responses. In addition to cancer, immune checkpoints are exploited in chronic infectious diseases. In human immunodeficiency virus (HIV) infection, the immune checkpoint molecule called programmed cell death protein 1 (PD-1) has been determined as being a major regulatory factor for T cell exhaustion. Recent studies with antibodies blocking either PD-1 ligand 1 (PD-L1) or PD-1 show not only promising results in the enhancement of HIV-specific immune responses but even in reducing the latent HIV reservoir. Apart from the therapeutic target for a functional cure of HIV-1, immune checkpoint molecules might be used as biomarkers for monitoring disease progression and therapeutic response. In this review, we will summarize and discuss the inhibitory immune checkpoint molecules PD-1, cytotoxic T-lymphocyte-associated protein 4 (CTLA4), lymphocyte-activation gene 3 (LAG3), and T cell immunoglobulin and mucin-domain-containing-3 (TIM3) as well as the co-stimulatory molecules CD40L and CD70, including their role in immunity, with a particular focus on HIV infection, and being potential targets for a functional HIV cure. View Full-Text
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Sperk, M.; Domselaar, R.V.; Neogi, U. Immune Checkpoints as the Immune System Regulators and Potential Biomarkers in HIV-1 Infection. Int. J. Mol. Sci. 2018, 19, 2000.
Sperk M, Domselaar RV, Neogi U. Immune Checkpoints as the Immune System Regulators and Potential Biomarkers in HIV-1 Infection. International Journal of Molecular Sciences. 2018; 19(7):2000.Chicago/Turabian Style
Sperk, Maike; Domselaar, Robert V.; Neogi, Ujjwal. 2018. "Immune Checkpoints as the Immune System Regulators and Potential Biomarkers in HIV-1 Infection." Int. J. Mol. Sci. 19, no. 7: 2000.
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