Evidence map›Paper›PMID 23422746›Full record

ArticleBlood2013

Impaired T-cell responses to sphingosine-1-phosphate in HIV-1 infected lymph nodes.

Joseph C Mudd, Patrick Murphy, Maura Manion, Robert Debernardo, Jeffrey Hardacre, John Ammori, Gareth A Hardy, Clifford V Harding, Ganapati H Mahabaleshwar, Mukesh K Jain and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2013. 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 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

27 citing papers in PubMed, 35 citations in OpenAlex.

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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

20 authors at 7 institutions in 1 country.

Joseph C MuddDivision of Infectious Diseases, Center for AIDS Research, Case Western Reserve University/UniversityHospitals Case Medical Center, Cleveland, OH 44106, USA.
Patrick Murphy
Maura Manion
Robert Debernardo
Jeffrey Hardacre
John Ammori
Gareth A Hardy
Clifford V Harding
Ganapati H Mahabaleshwar
Mukesh K Jain
Jeffrey M Jacobson
Ari D Brooks
Sharon Lewis
Timothy W Schacker
Jodi Anderson
Elias K Haddad
Rafael A Cubas
Benigno Rodriguez
Scott F Sieg
Michael M Lederman
Johns Hopkins University Center for AIDS ResearchDrexel University · USUniversity Hospitals Case Medical Center · USCase Western Reserve University · USUniversity of Minnesota · USVaccine and Gene Therapy InstituteVaccine & Gene Therapy Institute of Florida · US

Funding

WG3: HIV, Co-infections and Co-morbiditiesP30AI036219 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI Sharon L. Hillier, JONATHAN KARN · 1994 to 2026
$50.0M
TRANSLATIONAL RESEARCH ONCOLOGY TRAINING GRANTK12CA076917 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI GERSON, STANTON L. · 1997 to 2022
$14.2M
Specimen Acquisition and Distribution CoreP01AI076174 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI LEDERMAN, MICHAEL MARCEL · 2008 to 2012
$10.9M
Immunology Training Program-PredoctoralT32AI089474 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI COBB, BRIAN A · 2010 to 2025
$3.4M
KLF4 , the endothelium, and vascular inflammationR01HL097593 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI JAIN, MUKESH KUMAR · 2010 to 2013
$1.5M
NCI NIH HHS K12 CA076917NHLBI NIH HHS R01 HL097593NIAID NIH HHS P01 AI076174NIAID NIH HHS P30 AI036219NIAID NIH HHS T32 AI089474
6 · The paper itself

Abstract

The determinants of HIV-1-associated lymphadenopathy are poorly understood. We hypothesized that lymphocytes could be sequestered in the HIV-1+ lymph node (LN) through impairments in sphingosine-1-phosphate (S1P) responsiveness. To test this hypothesis, we developed novel assays for S1P-induced Akt phosphorylation and actin polymerization. In the HIV-1+ LN, naïve CD4 T cells and central memory CD4 and CD8 T cells had impaired Akt phosphorylation in response to S1P, whereas actin polymerization responses to S1P were impaired dramatically in all LN maturation subsets. These defects were improved with antiretroviral therapy. LN T cells expressing CD69 were unable to respond to S1P in either assay, yet impaired S1P responses were also seen in HIV-1+ LN T cells lacking CD69 expression. Microbial elements, HIV-1, and interferon α - putative drivers of HIV-1 associated immune activation all tended to increase CD69 expression and reduce T-cell responses to S1P in vitro. Impairment in T-cell egress from lymph nodes through decreased S1P responsiveness may contribute to HIV-1-associated LN enlargement and to immune dysregulation in a key organ of immune homeostasis.

Indexed as

AdultAgedAged, 80 and overAnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteAnti-Retroviral AgentsCD69 AntigensCell Line, TumorCells, CulturedFemaleFlow CytometryGene ExpressionHIV-1HIV InfectionsHumansAntigens, CDAntigens, Differentiation, T-LymphocyteAnti-Retroviral AgentsCD69 AntigensLectins, C-TypeLysophospholipidsProto-Oncogene Proteins c-aktReceptors, LysosphingolipidS1PR1 protein, humanSphingosinesphingosine 1-phosphateSphingosine-1-Phosphate Receptors

Identifiers

PMID23422746
PMCPMC3624937
OpenAlexW2010423053

What OpenQuestion holds

Textmetadata
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.