Evidence map›Paper›PMID 21788441›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

FTY720 blocks egress of T cells in part by abrogation of their adhesion on the lymph node sinus.

Liang Zhi, Pilhan Kim, Brian D Thompson, Costas Pitsillides, Alexander J Bankovich, Seok-Hyun Yun, Charles P Lin, Jason G Cyster, Mei X Wu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. VSVNature communications · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Loss of GαScientific reports · 2017
    Article
  14. Down-Regulation of CD62L Shedding in T Cells by CD39The Journal of investigative dermatology · 2017
    Article
  15. Article
  16. Article
  17. T cell-intrinsic S1PR1 regulates endogenous effector T-cell egress dynamics from lymph nodes during infection.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  18. Article
  19. Article
  20. Review
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

9 authors at 4 institutions in 1 country.

Liang ZhiWellman Center for Photomedicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Pilhan Kim
Brian D Thompson
Costas Pitsillides
Alexander J Bankovich
Seok-Hyun Yun
Charles P Lin
Jason G Cyster
Mei X Wu
Harvard University · USMassachusetts General Hospital · USHoward Hughes Medical Institute · USUniversity of San Francisco · US

Funding

Autoimmunity in IEX-1- transgenic miceR01AI050822 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI WU, MEI X · 2003 to 2006
$1.3M
IEX-1 in bridge of innate to adaptive immune responses to memory T cellsK02AI070785 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI WU, MEI X · 2006 to 2010
$531k
NIAID NIH HHS AI050822NIAID NIH HHS AI070785NIAID NIH HHS K02 AI070785NIAID NIH HHS R01 AI050822
6 · The paper itself

Abstract

Egress of lymphocytes from lymphoid tissues is a complex process in which Gαi-mediated signals play a decisive role. We show here that although FTY720, an agonist of the sphingosine 1-phosphate (S1P)(1) receptor, induces S1P(1) receptor internalization sufficiently in the presence or absence of Gαi2 or Gαi3, the drug blocks egress of wild-type (WT) and Gαi3-deficent T cells, but not Gαi2-deficient T cells, in both WT and Gαi2-deficient hosts. Intravital imaging of lymph nodes revealed that all three groups of T cells approached and engaged cortical sinusoids similarly in the presence or absence of FTY720. The cells also entered and departed the sinus at an almost identical frequency in the absence of the drug. However, after engagement of the sinus, most WT and Gαi3-deficient T cells retracted and migrated back into the parenchyma in FTY720-treated animals, due to a failure of the cells to establish adhesion on the sinus, whereas Gαi2-deficient T cells adhered firmly on the sinus, which prevented their retraction, facilitating their transmigration of the lymphatic endothelial barrier. These data confirm egress of Gαi2(-/-) T cells independent of S1P-mediated chemotaxis and failure of FTY720 to close lymphatic stromal channels and argue for the first time, to our knowledge, that FTY720 induces lymphopenia in part by impairing T cell adhesion to the sinus in a manner dependent on Gαi2.

Indexed as

AnimalsCell AdhesionCell SeparationChemotaxis, LeukocyteFingolimod HydrochlorideFlow CytometryGTP-Binding Protein alpha Subunit, Gi2Immunosuppressive AgentsLymph NodesMiceMice, KnockoutPropylene GlycolsReceptors, LysosphingolipidSphingosineT-LymphocytesFingolimod HydrochlorideGTP-Binding Protein alpha Subunit, Gi2Immunosuppressive AgentsPropylene GlycolsReceptors, LysosphingolipidSphingosine

Identifiers

PMID21788441
PMCPMC3167479
OpenAlexW2171316388

What OpenQuestion holds

Textmetadata
LicenceTDM
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.