Evidence map›Paper›PMID 21187439›Full record

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

In situ B cell-mediated immune responses and tubulointerstitial inflammation in human lupus nephritis.

Anthony Chang, Scott G Henderson, Daniel Brandt, Ni Liu, Riteesha Guttikonda, Christine Hsieh, Natasha Kaverina, Tammy O Utset, Shane M Meehan, Richard J Quigg and 2 more

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 207 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
207citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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

207 citing papers in PubMed, 1 synthesis or guideline pooled it, 344 citations in OpenAlex.

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  19. Can we cure autoimmunity?Current opinion in immunology · 2026
    Review
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147 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 1 country.

Anthony ChangDepartment of Pathology, University of Chicago, Chicago, IL 60637, USA.
Scott G Henderson
Daniel Brandt
Ni Liu
Riteesha Guttikonda
Christine Hsieh
Natasha Kaverina
Tammy O Utset
Shane M Meehan
Richard J Quigg
Eric Meffre
Marcus R Clark
University of Chicago · USCornell University · US

Funding

University of Chicago Autoimmunity Center of ExcellenceU19AI082724 · NIAID · UNIVERSITY OF CHICAGO · PI CLARK, MARCUS RAMSAY · 2009 to 2023
$7.2M
Loss of B Cell Tolerance in Rheumatoid ArthritisR01AI071087 · NIAID · YALE UNIVERSITY · PI MEFFRE, ERIC · 2006 to 2016
$4.3M
Tertiary Lymphoid Neogenesis in Human Lupus NephritisR01AR055646 · NIAMS · UNIVERSITY OF CHICAGO · PI CLARK, MARCUS RAMSAY · 2008 to 2018
$3.4M
Impact of regulatory T cells on human peripheral B cell toleranceR21AI095848 · NIAID · YALE UNIVERSITY · PI MEFFRE, ERIC · 2012 to 2013
$457k
NIAID NIH HHS AI082724NIAID NIH HHS R01 AI071087NIAID NIH HHS R21 AI095848NIAID NIH HHS U19 AI082724NIAMS NIH HHS AR055646NIAMS NIH HHS R01 AR055646
6 · The paper itself

Abstract

The most prevalent severe manifestation of systemic lupus erythematosus is nephritis, which is characterized by immune complex deposition, inflammation, and scarring in glomeruli and the tubulointerstitium. Numerous studies indicated that glomerulonephritis results from a systemic break in B cell tolerance, resulting in the local deposition of immune complexes containing Abs reactive with ubiquitous self-Ags. However, the pathogenesis of systemic lupus erythematosus tubulointerstitial disease is not known. In this article, we demonstrate that in more than half of a cohort of 68 lupus nephritis biopsies, the tubulointerstitial infiltrate was organized into well-circumscribed T:B cell aggregates or germinal centers (GCs) containing follicular dendritic cells. Sampling of the in situ-expressed Ig repertoire revealed that both histological patterns were associated with intrarenal B cell clonal expansion and ongoing somatic hypermutation. However, in the GC histology, the proliferating cells were CD138(-)CD20(+) centroblasts, whereas they were CD138(+)CD20(low/-) plasmablasts in T:B aggregates. The presence of GCs or T:B aggregates was strongly associated with tubular basement membrane immune complexes. These data implicate tertiary lymphoid neogenesis in the pathogenesis of lupus tubulointerstitial inflammation.

Indexed as

Adaptive ImmunityAdolescentAdultAmino Acid SequenceBase SequenceB-Lymphocyte SubsetsCell MovementChildChild, PreschoolClone CellsDendritic Cells, FollicularFemaleGerminal CenterHumansInfantInflammation

Identifiers

PMID21187439
PMCPMC3124090
OpenAlexW2123082276

What OpenQuestion holds

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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.