Evidence map›Paper›PMID 29778672›Full record

ArticleCytokine2018

Defective MyD88 and IRAK4 but not TLR-2 expression in HIV+ individuals with latent tuberculosis infection.

Kamakshi Prudhula Devalraju, Venkata Sanjeev Kumar Neela, Ramulu Gaddam, Arunabala Chaudhury, Abhinav Van, Siva Sai Krovvidi, Ramakrishna Vankayalapati, Vijaya Lakshmi Valluri

Open access · greenAbstract read
In one paragraph

Article in Cytokine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. A Role of Intracellular Toll-Like Receptors (3, 7, and 9) in Response toInternational journal of molecular sciences · 2020
    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

8 authors at 3 institutions in 2 countries.

Kamakshi Prudhula DevalrajuImmunology and Molecular Biology Division, Blue Peter Public Health and Research Centre, LEPRA Society, Cherlapally, Hyderabad 501301, India.
Venkata Sanjeev Kumar NeelaImmunology and Molecular Biology Division, Blue Peter Public Health and Research Centre, LEPRA Society, Cherlapally, Hyderabad 501301, India.
Ramulu GaddamDepartment of Respiratory Medicine, AP Chest and General Hospital, Osmania Medical College, Erragadda, Hyderabad 500038, India.
Arunabala ChaudhuryClinical Division, Cheyutha, LEPRA Society, Cherlapally, Hyderabad 501301, India.
Abhinav VanDepartment of Pulmonary Immunology, Center for Biomedical Research, University of Texas Health Center, Tyler, TX 75708, United States.
Siva Sai KrovvidiDepartment of Biotechnology, Sreenidhi Institute of Science and Technology, Yamnampet, Ghatkesar, Hyderabad, Telangana 501301, India.
Ramakrishna VankayalapatiDepartment of Pulmonary Immunology, Center for Biomedical Research, University of Texas Health Center, Tyler, TX 75708, United States. Electronic address: krishna.vankayalapati@uthct.edu.
Vijaya Lakshmi ValluriImmunology and Molecular Biology Division, Blue Peter Public Health and Research Centre, LEPRA Society, Cherlapally, Hyderabad 501301, India. Electronic address: vijayavalluri@gmail.com.
Lepra Society · INThe University of Texas Health Science Center at Tyler · USOsmania Medical College · IN

Funding

IFN-γ independent inhibition of MTB growth in human macrophagesR01AI123310 · NIAID · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI VANKAYALAPATI, RAMAKRISHNA · 2017 to 2020
$1.6M
Monocyte subpopulation in HIV+LTB+ individuals and development of active TBR21AI127178 · NIAID · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI VANKAYALAPATI, RAMAKRISHNA · 2016 to 2017
$393k
T-regs mediated immune responses in LTBI HIV positive individualsR21AI120257 · NIAID · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI VANKAYALAPATI, RAMAKRISHNA · 2015 to 2016
$386k
NIAID NIH HHS R01 AI123310NIAID NIH HHS R21 AI120257NIAID NIH HHS R21 AI127178
6 · The paper itself

Abstract

HIV infection markedly increases the likelihood of latent tuberculosis infection progressing to active TB. Information on expression of TLR-2, myeloid differentiation factor (MyD88), IL-1R- associated kinase-4 (IRAK4) and nuclear factor kappa B (NF-kB) in HIV+LTBI+ and HIV+ patients with active TB disease is limited. We found significantly higher percentages of CD14+TLR2+ cells in PBMCs of HIV+LTBI+ patients compared to HIV-LTBI+ individuals. γ-irradiated Mtb was unable to induce MyD88, IRAK4 expression and IL-1β, MCP-1, IP-10 production in HIV+LTBI+ patients. Pleural fluids from HIV+TB+ patients had low IL-1β, MCP-1, IP-10 and high IL-10, TNF-α production. γ-irradiated Mtb stimulated CD14+ cells from HIV+TB+ patients had low IL-1β, MCP-1, IP-10 production and MyD88, IRAK4 and similar NF-kB expression compared to those from of HIV-TB+ patients. Our results suggest defective MyD88, IRAK4 but not NF-kB inhibit IL-1β, MCP-1 and IP-10 production by CD14+ cells of HIV+ individuals with LTBI and active TB disease in peripheral blood and at the site of disease.

Indexed as

Cell LineChemokine CCL2Chemokine CXCL10HIV InfectionsHumansInterleukin-1betaInterleukin-1 Receptor-Associated KinasesLatent TuberculosisLipopolysaccharide ReceptorsMycobacterium tuberculosisMyeloid Differentiation Factor 88Signal TransductionToll-Like Receptor 2Chemokine CCL2Chemokine CXCL10Interleukin-1betaInterleukin-1 Receptor-Associated KinasesIRAK4 protein, humanLipopolysaccharide ReceptorsMYD88 protein, humanMyeloid Differentiation Factor 88TLR2 protein, humanToll-Like Receptor 2CytokinesHIVHumanMonocytesTLR-2Tuberculosis

Identifiers

PMID29778672
PMCPMC6103807
OpenAlexW2804579289

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.