Evidence map›Paper›PMID 27725666›Full record

ArticleImmunology and cell biology2017

Protein tyrosine phosphatase PTPN22 has dual roles in promoting pathogen versus homeostatic-driven CD8 T-cell responses.

Tatiana Jofra, Roberta Di Fonte, Tarun Edgar Hutchinson, Farhad Dastmalchi, Giuseppe Galvani, Manuela Battaglia, Shahram Salek-Ardakani, Georgia Fousteri

Abstract read
PubMed Publisher
In one paragraph

Article in Immunology and cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. An autoimmunity-associated allele ofProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  3. An Autoimmunity-associated allele ofbioRxiv : the preprint server for biology · 2025
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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

8 authors at 4 institutions in 2 countries.

Tatiana JofraDivision of Immunology Transplantation and Infectious Diseases (DITID), Diabetes Research Institute (DRI), IRCCS San Raffaele Scientific Institute, Milan, Italy.
Roberta Di FonteDivision of Immunology Transplantation and Infectious Diseases (DITID), Diabetes Research Institute (DRI), IRCCS San Raffaele Scientific Institute, Milan, Italy.
Tarun Edgar HutchinsonDepartment of Pathology, Immunology & Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Farhad DastmalchiDepartment of Pathology, Immunology & Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Giuseppe GalvaniDivision of Immunology Transplantation and Infectious Diseases (DITID), Diabetes Research Institute (DRI), IRCCS San Raffaele Scientific Institute, Milan, Italy.
Manuela BattagliaDivision of Immunology Transplantation and Infectious Diseases (DITID), Diabetes Research Institute (DRI), IRCCS San Raffaele Scientific Institute, Milan, Italy.
Shahram Salek-ArdakaniDepartment of Pathology, Immunology & Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Georgia FousteriDivision of Immunology Transplantation and Infectious Diseases (DITID), Diabetes Research Institute (DRI), IRCCS San Raffaele Scientific Institute, Milan, Italy.
University of Florida · USVita-Salute San Raffaele University · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITIstituto di Ricovero e Cura a Carattere Scientifico San Raffaele

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PTPN22 (protein tyrosine phosphatase non receptor 22) encodes a tyrosine phosphatase that functions as a key regulator of immune homeostasis. In particular, PTPN22 inhibits T-cell receptor signaling and selectively promotes type I interferon responses in myeloid cells. To date, there is little information on the CD8 T-cell-intrinsic role of PTPN22 in response to a viral pathogen. We unexpectedly found that PTPN22-deficient virus-specific CD8 T cells failed to accumulate in wild-type hosts after lymphocytic choriomeningitis virus infection. Lack of PTPN22 expression altered CD8 T-cell activation and antiviral cytokine production, but did not significantly affect the composition of effector and memory cell precursors. Most significantly, in vivo, PTPN22-deficient CD8 T cells showed a profound defect in upregulating STAT-1 after lymphocytic choriomeningitis virus infection and considerably less phosphorylation of STAT-1 in response to IFN-α treatment in vitro compared with their wild-type counterparts. In stark contrast, following transfer into lymphopenic mice, CD8 T-cell expansion and central-like phenotype, was considerably increased in the absence of PTPN22. Collectively, our results suggest that PTPN22 has dual roles in T-cell clonal expansion and effector function; whereas it promotes antigen-driven responses during acute infection by positively regulating interferon signaling in T cells, PTPN22 inhibits homeostatic-driven proliferation.

Indexed as

HomeostasisAnimalsBiomarkersCD8-Positive T-LymphocytesCell ProliferationCytokinesInterferon Type ILymphocyte ActivationLymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMice, Inbred C57BLPhosphorylationProtein Tyrosine Phosphatase, Non-Receptor Type 22Signal TransductionSTAT1 Transcription FactorUp-RegulationBiomarkersCytokinesInterferon Type IProtein Tyrosine Phosphatase, Non-Receptor Type 22Ptpn22 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID27725666
OpenAlexW2530190632

What OpenQuestion holds

Textmetadata
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Registered trials

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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.