Evidence map›Paper›PMID 21433035›Full record

ReviewMedicinal research reviews2012

Antigen-specific blocking of CD4-specific immunological synapse formation using BPI and current therapies for autoimmune diseases.

Prakash Manikwar, Paul Kiptoo, Ahmed H Badawi, Barlas Büyüktimkin, Teruna J Siahaan

Open access · bronzeAbstract readReview
In one paragraph

Review in Medicinal research reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-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

25 citing papers in PubMed, 33 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

5 authors at 1 institution in 1 country.

Prakash ManikwarDepartment of Pharmaceutical Chemistry, University of Kansas, Lawrence, KA 66047, USA.
Paul Kiptoo
Ahmed H Badawi
Barlas Büyüktimkin
Teruna J Siahaan
University of Kansas · US

Funding

Tergeting LFA-1 for Delivering Antigenic PeptidesR56AI063002 · NIAID · UNIVERSITY OF KANSAS LAWRENCE · PI SIAHAAN, TERUNA J. · 2010 to 2010
$358k
NIAID NIH HHS R56 AI063002
6 · The paper itself

Abstract

In this review, we discuss T-cell activation, etiology, and the current therapies of autoimmune diseases (i.e., MS, T1D, and RA). T-cells are activated upon interaction with antigen-presenting cells (APC) followed by a "bull's eye"-like formation of the immunological synapse (IS) at the T-cell-APC interface. Although the various disease-modifying therapies developed so far have been shown to modulate the IS and thus help in the management of these diseases, they are also known to present some undesirable side effects. In this study, we describe a novel and selective way to suppress autoimmunity by using a bifunctional peptide inhibitor (BPI). BPI uses an intercellular adhesion molecule-1 (ICAM-1)-binding peptide to target antigenic peptides (e.g., proteolipid peptide, glutamic acid decarboxylase, and type II collagen) to the APC and therefore modulate the immune response. The central hypothesis is that BPI blocks the IS formation by simultaneously binding to major histocompatibility complex-II and ICAM-1 on the APC and selectively alters the activation of T cells from T(H)1 to T(reg) and/or T(H)2 phenotypes, leading to tolerance.

Indexed as

AnimalsAntigen-Presenting CellsAutoimmune DiseasesCD4 AntigensCollagen Type IIGlutamate DecarboxylaseHumansImmunological SynapsesIntercellular Adhesion Molecule-1Models, BiologicalPeptidesT-LymphocytesCD4 AntigensCollagen Type IIGlutamate DecarboxylaseIntercellular Adhesion Molecule-1Peptides

Identifiers

PMID21433035
PMCPMC4441537
OpenAlexW1750613264

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.