Immune Checkpoints as the Immune System Regulators and Potential Biomarkers in HIV-1 Infection

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Term Occurence Count Dictionary
cysticercosis 2 infectiousdiseases
hepatitis B 2 infectiousdiseases
hepatitis C 1 infectiousdiseases
infectious disease 4 infectiousdiseases
malaria 6 infectiousdiseases
schistosomiasis 2 infectiousdiseases
tuberculosis 4 infectiousdiseases
AIDS 6 infectiousdiseases

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AIDS 14963 and these cells deplete over time when patients progress towards acquired immunodeficiency syndrome ( AIDS ) [[33]]. This results in inadequate pathogen-specific CD4+ T cell responses, including HIV-specific
AIDS 22106 production and surface expression on CD4+ T cells during progressing disease and/or the development of AIDS . At the same time, CD4+ T cell effector functions, for example IL-12 production, were impaired [[50],[51],[52]].
AIDS 23802 patient more susceptible to opportunistic infections as similarities are observed between patients with AIDS and those having congenital CD40L deficiencies. Thus, therapies preventing and reversing the drop of
AIDS 24834 to lead to exhaustion of T cells, which may contribute to immune deficiency during HIV infection and AIDS [[56]]. In concordance with our study, Lantto et al. found higher frequencies of CD4+ CD70+ expressing
AIDS 26269 CTLA4, being the pioneer in immune checkpoint therapy in cancer, is much less appreciated in HIV and AIDS . Some groups reported an up-regulation of CTLA4 on HIV-specific CD4+ T cells that are associated with
AIDS 36614 immune exhaustion and the role of immune checkpoint molecules, the similarities between cancer and AIDS are quite astonishing. In both diseases, T cells are challenged with chronic antigen exposure that results
cysticercosis 8947 promising. In worm infections, both Schistosoma mansoni and Taenia crassiceps, causing schistosomiasis or cysticercosis respectively, up-regulate PD-L1 expression on macrophages in mice during infection. In this way, T cell
cysticercosis 9202 diseases. Importantly, blockade of PD-L1 in schistosomiasis and blockade of PD-1, PD-L1, or PD-L2 in cysticercosis , blocked the ability of macrophages to induce T cell anergy and restored T cell proliferation in mice
hepatitis B 9356 induce T cell anergy and restored T cell proliferation in mice [[22],[23]].Several viruses including hepatitis B virus (HBV), hepatitis C virus (HCV), and HIV are responsible for chronic infectious diseases. Thus,
hepatitis B 9614 of immune checkpoints has been described in those aforementioned infections [[16]]. During chronic hepatitis B infection (CHB), PD-1 is considered as the dominant inhibitory receptor that can be targeted for therapy.
hepatitis C 9381 restored T cell proliferation in mice [[22],[23]].Several viruses including hepatitis B virus (HBV), hepatitis C virus (HCV), and HIV are responsible for chronic infectious diseases. Thus, it is not surprising that
infectious disease 927 down-regulate anti-tumor responses. In addition to cancer, immune checkpoints are exploited in chronic infectious disease s. In human immunodeficiency virus (HIV) infection, the immune checkpoint molecule called programmed
infectious disease 6075 checkpoints play a crucial role in regulating immune responses against invading pathogens, their part in infectious disease s has been increasingly discussed in the last decade. T cells are persistently exposed to antigens in
infectious disease 9442 viruses including hepatitis B virus (HBV), hepatitis C virus (HCV), and HIV are responsible for chronic infectious disease s. Thus, it is not surprising that aberrant expression of immune checkpoints has been described in those
infectious disease 12466 blocking these pathways could be a major immunotherapeutic strategy in (functionally) curing the chronic infectious disease s, as is currently being developed for cancer therapies.3. Programmed Cell Death Protein 1 (PD-1) Signaling
malaria 5656 levels of PD-1 and other immune checkpoints might also serve as prognostic biomarkers in tuberculosis, malaria , and chronic viral infections.In this review, we will summarize and discuss selected immune checkpoints
malaria 7741 Concerning protozoa infections, the unicellular parasite Plasmodium falciparum is the causing agent of malaria tropica. In Kenyan children who are persistently exposed to this pathogen, a high expression of PD-1
malaria 8437 LAG3 expression on CD8+ T cells, higher frequencies of CD4+ T cells expressing PD-1 are observed in malaria -infected children in Mali. In a murine malaria model, blocking PD-1 pathway in combination with blocking
malaria 8484 frequencies of CD4+ T cells expressing PD-1 are observed in malaria-infected children in Mali. In a murine malaria model, blocking PD-1 pathway in combination with blocking LAG3 signaling reduced parasitemia, improved
malaria 8783 extended survival of the mice [[21]]. No human trials with anti-PD-1 antibodies have been performed in malaria patients yet, but results from murine models seem promising. In worm infections, both Schistosoma mansoni
malaria 12277 expression of PD-1 and other immune checkpoints might serve as prognostic biomarkers in tuberculosis, malaria , and chronic viral infections. In combination with standard drug treatment, blocking these pathways
schistosomiasis 8928 models seem promising. In worm infections, both Schistosoma mansoni and Taenia crassiceps, causing schistosomiasis or cysticercosis respectively, up-regulate PD-L1 expression on macrophages in mice during infection.
schistosomiasis 9145 In this way, T cell proliferation was inhibited in both diseases. Importantly, blockade of PD-L1 in schistosomiasis and blockade of PD-1, PD-L1, or PD-L2 in cysticercosis, blocked the ability of macrophages to induce
tuberculosis 5642 and protein levels of PD-1 and other immune checkpoints might also serve as prognostic biomarkers in tuberculosis , malaria, and chronic viral infections.In this review, we will summarize and discuss selected immune
tuberculosis 6940 different species including bacteria, protists, and animals [[15],[16]]. In patients with active human tuberculosis (TB) caused by Mycobacterium tuberculosis, the number of PD-1 expressing cells in peripheral blood was
tuberculosis 6982 protists, and animals [[15],[16]]. In patients with active human tuberculosis (TB) caused by Mycobacterium tuberculosis , the number of PD-1 expressing cells in peripheral blood was elevated, and expression of PD-L1 was also
tuberculosis 12263 concluded that the expression of PD-1 and other immune checkpoints might serve as prognostic biomarkers in tuberculosis , malaria, and chronic viral infections. In combination with standard drug treatment, blocking these

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