Evidence map›Paper›PMID 25926831›Full record

ArticleFrontiers in immunology2015

Negative Regulation of Humoral Immunity Due to Interplay between the SLAMF1, SLAMF5, and SLAMF6 Receptors.

Ninghai Wang, Peter J Halibozek, Burcu Yigit, Hui Zhao, Michael S O'Keeffe, Peter Sage, Arlene Sharpe, Cox Terhorst

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  14. Observational
  15. Article
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  17. Article
  18. SLAMF9 regulates pDC homeostasis and function in health and disease.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  19. Review
  20. Article
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 2 institutions in 1 country.

Ninghai WangDivision of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School , Boston, MA , USA.
Peter J HalibozekDivision of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School , Boston, MA , USA.
Burcu YigitDivision of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School , Boston, MA , USA.
Hui ZhaoDivision of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School , Boston, MA , USA.
Michael S O'KeeffeDivision of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School , Boston, MA , USA.
Peter SageDepartment of Microbiology and Immunology, Harvard Medical School , Boston, MA , USA.
Arlene SharpeDepartment of Microbiology and Immunology, Harvard Medical School , Boston, MA , USA.
Cox TerhorstDivision of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School , Boston, MA , USA.
Harvard University · USBeth Israel Deaconess Medical Center · US

Funding

The Slamf3, Slamf5, and Slamf6 receptor-induced pathways to murine lupusP01AI065687 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TERHORST, CORNELIS P · 2006 to 2016
$14.7M
NIAID NIH HHS P01 AI065687
6 · The paper itself

Abstract

Whereas the SLAMF-associated protein (SAP) is involved in differentiation of T follicular helper (Tfh) cells and antibody responses, the precise requirements of SLAMF receptors in humoral immune responses are incompletely understood. By analyzing mice with targeted disruptions of the Slamf1, Slamf5, and Slamf6 genes, we found that both T-dependent and T-independent antibody responses were twofold higher compared to those in single knockout mice. These data suggest a suppressive synergy of SLAMF1, SLAMF5, and SLAMF6 in humoral immunity, which contrasts the decreased antibody responses resulting from a defective GC reaction in the absence of the adapter SAP. In adoptive co-transfer assays, both [Slamf1 + 5 + 6] (-/-) B and T cells were capable of inducing enhanced antibody responses, but more pronounced enhancement was observed after adoptive transfer of [Slamf1 + 5 + 6] (-/-) B cells compared to that of [Slamf1 + 5 + 6] (-/-) T cells. In support of [Slamf1 + 5 + 6] (-/-) B cell intrinsic activity, [Slamf1 + 5 + 6] (-/-) mice also mounted significantly higher antibody responses to T-independent type 2 antigen. Furthermore, treatment of mice with anti-SLAMF6 monoclonal antibody results in severe inhibition of the development of Tfh cells and GC B cells, confirming a suppressive effect of SLAMF6. Taken together, these results establish SLAMF1, SLAMF5, and SLAMF6 as important negative regulators of humoral immune response, consistent with the notion that SLAM family receptors have dual functions in immune responses.

Indexed as

anti-SLAMF6 mAbfollicular T helper cellsgerminal center B cellsmarginal zone B cellsSLAM-associated proteinSLAM family receptors

Identifiers

PMID25926831
PMCPMC4396446
OpenAlexW1994826373

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Registered trials

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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.