ArticleProceedings of the National Academy of Sciences of the United States of America2016
PTPN22 contributes to exhaustion of T lymphocytes during chronic viral infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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.
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.
Who cites it
36 citing papers in PubMed, 48 citations in OpenAlex.
- β-Adrenergic receptors as immunomodulators in T cells: mechanisms of neuroimmune crosstalk and pathophysiological implications.Molecular medicine (Cambridge, Mass.) · 2026Review
- A CREM-ITGA2B-MAPK axis drives proliferation and invasiveness in gastric cancer: insights from single-cell analysis.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- An autoimmunity-associated allele ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Type I interferon production in myeloid cells is regulated by factors independent of Ptpn22.ImmunoHorizons · 2025Article
- An Autoimmunity-associated allele ofbioRxiv : the preprint server for biology · 2025Article
- Longitudinal single cell profiling of epitope specific memory CD4+ T cell responses to recombinant zoster vaccine.Nature communications · 2025Article
- Article
- A novel gain-of-function phosphorylation site modulates PTPN22 inhibition of TCR signaling.The Journal of biological chemistry · 2024Article
- Autoimmunity-associated allele of tyrosine phosphatase gene PTPN22 enhances anti-viral immunity.PLoS pathogens · 2024Article
- Regulation of T Cell Signaling and Immune Responses by PTPN22.Molecular and cellular biology · 2024Review
- Article
- The βNature · 2023Article
- Article
- Article
- VISTA Targeting of T-cell Quiescence and Myeloid Suppression Overcomes Adaptive Resistance.Cancer immunology research · 2023Article
- PTPN22: structure, function, and developments in inhibitor discovery with applications for immunotherapy.Expert opinion on drug discovery · 2022Review
- Regulation of activated T cell survival in rheumatic autoimmune diseases.Nature reviews. Rheumatology · 2022Review
- Functional Impact of Risk Gene Variants on the Autoimmune Responses in Type 1 Diabetes.Frontiers in immunology · 2022Review
- CD4 T-Cell Exhaustion: Does It Exist and What Are Its Roles in Cancer?Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Review
- Chronic LCMV Infection Is Fortified with Versatile Tactics to Suppress Host T Cell Immunity and Establish Viral Persistence.Viruses · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The protein encoded by the autoimmune-associated protein tyrosine phosphatase nonreceptor type 22 gene, PTPN22, has wide-ranging effects in immune cells including suppression of T-cell receptor signaling and promoting efficient production of type I interferons (IFN-I) by myeloid cells. Here we show that mice deficient in PTPN22 resist chronic viral infection with lymphocytic choriomeningitis virus clone 13 (LCMV cl13). The numbers and function of viral-specific CD4 T lymphocytes is greatly enhanced, whereas expression of the IFNβ-induced IL-2 repressor, cAMP-responsive element modulator (CREM) is reduced. Reduction of CREM expression in wild-type CD4 T lymphocytes prevents the loss of IL-2 production by CD4 T lymphocytes during infection with LCMV cl13. These findings implicate the IFNβ/CREM/IL-2 axis in regulating T-lymphocyte function during chronic viral infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.