Evidence map›Paper›PMID 21918197›Full record

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

Anti-CD180 (RP105) activates B cells to rapidly produce polyclonal Ig via a T cell and MyD88-independent pathway.

Jay W Chaplin, Shinji Kasahara, Edward A Clark, Jeffrey A Ledbetter

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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

37 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
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  4. Blunting specific T-dependent antibody responses with engineered "decoy" B cells.Molecular therapy : the journal of the American Society of Gene Therapy · 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

4 authors at 1 institution in 1 country.

Jay W ChaplinDivision of Rheumatology, Department of Medicine; University of Washington, Seattle, WA 98195, USA. jchaplin@u.washington.edu
Shinji Kasahara
Edward A Clark
Jeffrey A Ledbetter
University of Washington · US

Funding

TRAINING IN MOLECULAR AND CELLULAR BIOLOGYT32GM007270 · NIGMS · UNIVERSITY OF WASHINGTON · PI RAIBLE, DAVID W · 1985 to 2020
$21.0M
Programming protective immunity by targeting antigens to the CD180 receptorR01AI052203 · NIAID · UNIVERSITY OF WASHINGTON · PI FULLER, DEBORAH H. · 2003 to 2019
$6.3M
FDRC1 AND FOLLICULAR DENDRITIC CELL SIGNALING PATHWAYSR37AI044257 · NIAID · UNIVERSITY OF WASHINGTON · PI CLARK, EDWARD A · 2004 to 2013
$4.0M
Role of B cell activating factor (BAFF) in B cell responses and autoimmunityR01AI044257 · NIAID · UNIVERSITY OF WASHINGTON · PI GILTIAY, NATALIA V · 1999 to 2020
$3.7M
CD180(RP105) Regulation of TLR and BCR Responses in B CellsR21AI085311 · NIAID · UNIVERSITY OF WASHINGTON · PI LEDBETTER, JEFFREY A · 2010 to 2011
$421k
NIAID NIH HHS AI44257NIAID NIH HHS AI52203NIAID NIH HHS AI85311NIAID NIH HHS R01 AI044257NIAID NIH HHS R01 AI052203NIAID NIH HHS R21 AI085311NIAID NIH HHS R37 AI044257NIGMS NIH HHS 2T32 GM007270NIGMS NIH HHS T32 GM007270
6 · The paper itself

Abstract

CD180 is homologous to TLR4 and regulates TLR4 signaling, yet its function is unclear. We report that injection of anti-CD180 mAb into mice induced rapid Ig production of all classes and subclasses, with the exception of IgA and IgG2b, with up to 50-fold increases in serum IgG1 and IgG3. IgG production after anti-CD180 injection was not due to reactivation of memory B cells and was retained in T cell-deficient (TCR knockout [KO]), CD40 KO, IL-4 KO, and MyD88 KO mice. Anti-CD180 rapidly increased both transitional and mature B cells, with especially robust increases in transitional B cell number, marginal zone B cell proliferation, and CD86, but not CD80, expression. In contrast, anti-CD40 induced primarily follicular B cell and myeloid expansion, with increases in expression of CD80 and CD95 but not CD86. The expansion of splenic B cells was due, in part, to proliferation and occurred in wild-type and TCR KO mice, whereas T cell expansion occurred in wild-type, but not in B cell-deficient, mice, indicating a direct role for B cells in CD180 stimulation in vivo. Combination of anti-CD180 with various MyD88-dependent TLR ligands biased B cell fate because coinjection diminished Ig production, but purified B cells exhibited synergistic proliferation. Anti-CD180 had no effect on cytokine production from B cells, but it increased IL-6, IL-10, and TNF-α production in combination with LPS or CpG. Thus, CD180 stimulation induces intrinsic B cell proliferation and differentiation, causing rapid increases in IgG, and integrates MyD88-dependent TLR signals to regulate proliferation, cytokine production, and differentiation.

Indexed as

AnimalsAntibody FormationAntigens, CDB-LymphocytesCell DifferentiationCell ProliferationCell SeparationEnzyme-Linked Immunosorbent AssayFlow CytometryImmunoglobulinsLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88T-LymphocytesAntigens, CDImmunoglobulinsLy78 protein, mouseMyd88 protein, mouseMyeloid Differentiation Factor 88

Identifiers

PMID21918197
PMCPMC3394853
OpenAlexW2129374292

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.