Evidence map›Paper›PMID 29987244›Full record

ReviewInternational journal of molecular sciences2018

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

Maike Sperk, Robert van Domselaar, Ujjwal Neogi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.6field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Can Soluble Immune Checkpoint Molecules on Exosomes Mediate Inflammation?Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Maike SperkDivision of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, 141 86 Stockholm, Sweden. maike.sperk@ki.se.ORCID 0000-0003-0320-6111
Robert van DomselaarDepartment of Medicine Huddinge, Unit of Infectious Diseases, Karolinska Institutet, Karolinska University Hospital, 141 86 Stockholm, Sweden. robert.van.domselaar.1@ki.se.
Ujjwal NeogiDivision of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, 141 86 Stockholm, Sweden. ujjwal.neogi@ki.se.ORCID 0000-0002-0844-3338
Karolinska Institutet · SEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune 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.

Indexed as

AntibodiesAntigens, CDB7-H1 AntigenBiomarkersCTLA-4 AntigenDisease ProgressionHepatitis A Virus Cellular Receptor 2HIV-1HIV InfectionsHumansLymphocyte Activation Gene 3 ProteinProgrammed Cell Death 1 ReceptorAntibodiesAntigens, CDB7-H1 AntigenBiomarkersCD274 protein, humanCTLA-4 AntigenCTLA4 protein, humanHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2Lymphocyte Activation Gene 3 ProteinPDCD1 protein, humanProgrammed Cell Death 1 Receptorbiomarkerhuman immunodeficiency virus (HIV)immune checkpointprogrammed cell death protein 1 (PD-1)T cell exhaustion

Identifiers

PMID29987244
PMCPMC6073446
OpenAlexW2876776741

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.