Evidence map›Paper›PMID 26856698›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

LAMP-2C Inhibits MHC Class II Presentation of Cytoplasmic Antigens by Disrupting Chaperone-Mediated Autophagy.

Liliana Pérez, Shawna McLetchie, Gail J Gardiner, Sarah N Deffit, Delu Zhou, Janice S Blum

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

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  10. Altered Splicing ofMedicina (Kaunas, Lithuania) · 2024
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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

6 authors at 3 institutions in 1 country.

Liliana PérezDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202;
Shawna McLetchieDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202;ORCID http://orcid.org/0000-0002-9853-0688
Gail J GardinerDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202;ORCID http://orcid.org/0000-0001-5306-572X
Sarah N DeffitMedical Sciences Program, Indiana University, Bloomington, IN 47405; and.
Delu ZhouDepartment of Pathology, University of Utah, Salt Lake City, UT 84112.
Janice S BlumDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202; jblum@iupui.edu.
Indiana University – Purdue University Indianapolis · USIndiana University Bloomington · USUniversity of Utah · US

Funding

BASIC SCIENCE STUDIES ON GENE THERAPY OF BLOOD DISEASEST32HL007910 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Roland W. Herzog, Reuben Kapur · 1999 to 2026
$7.6M
Immunology and Infectious Diseases Training ProgramT32AI060519 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MARK H KAPLAN · 2004 to 2026
$6.0M
CLASS II ANTIGEN PRESENTATION VIA CHAPERONE MEDIATED AUTOPHAGYR01AI079065 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI BLUM, JANICE S · 2010 to 2014
$1.8M
NHLBI NIH HHS T32 HL007910NHLBI NIH HHS T32HL007910NIAID NIH HHS R01 AI079065NIAID NIH HHS R01AI1079065NIAID NIH HHS T32 AI060519NIAID NIH HHS T32AI060519
6 · The paper itself

Abstract

Cells use multiple autophagy pathways to sequester macromolecules, senescent organelles, and pathogens. Several conserved isoforms of the lysosome-associated membrane protein-2 (LAMP-2) regulate these pathways influencing immune recognition and responses. LAMP-2A is required for chaperone-mediated autophagy (CMA), which promotes Ag capture and MHC class II (MHCII) presentation in B cells and signaling in T cells. LAMP-2B regulates lysosome maturation to impact macroautophagy and phagocytosis. Yet, far less is known about LAMP-2C function. Whereas LAMP2A and LAMP2B mRNA were broadly detected in human tissues, LAMP2C expression was more limited. Transcripts for the three LAMP2 isoforms increased with B cell activation, although specific gene induction varied depending on TLR versus BCR engagement. To examine LAMP-2C function in human B cells and specifically its role in Ag presentation, we used ectopic gene expression. Increased LAMP-2C expression in B cells did not alter MHCII expression or invariant chain processing, but did perturb cytoplasmic Ag presentation via CMA. MHCII presentation of epitopes from exogenous and membrane Ags was not affected by LAMP-2C expression in B cells. Similarly, changes in B cell LAMP-2C expression did not impact macroautophagy. The gene expression of other LAMP2 isoforms and proteasome and lysosomal proteases activities were unperturbed by LAMP-2C ectopic expression. LAMP-2C levels modulated the steady-state expression of several cytoplasmic proteins that are targeted for degradation by CMA and diminished peptide translocation via this pathway. Thus, LAMP-2C serves as a natural inhibitor of CMA that can selectively skew MHCII presentation of cytoplasmic Ags.

Indexed as

Antigen PresentationAutophagyB-LymphocytesCell SeparationCytoplasmElectroporationEnzyme-Linked Immunosorbent AssayFlow CytometryHistocompatibility Antigens Class IIHumansImmunoblottingImmunoprecipitationLysosomal-Associated Membrane Protein 2Protein IsoformsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionHistocompatibility Antigens Class IILAMP2 protein, humanLysosomal-Associated Membrane Protein 2Protein Isoforms

Identifiers

PMID26856698
PMCPMC4779666
OpenAlexW2272573169

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.