Galectin-9 ameliorates clinical severity of MRL/lpr lupus-prone mice by inducing plasma cell apoptosis independently of Tim-3. (Q34667834)

3 August 2017

title

Galectin-9 ameliorates clinical severity of MRL/lpr lupus-prone mice by inducing plasma cell apoptosis independently of Tim-3. (English)

1 reference

3 August 2017

6

Hirohito Mori

1 reference

3 August 2017

8

Tsutomu Masaki

1 reference

3 August 2017

Masahiro Moritoki

1

1 reference

3 August 2017

Takeshi Kadowaki

2

1 reference

3 August 2017

Toshiro Niki

3

1 reference

3 August 2017

Daisuke Nakano

4

1 reference

3 August 2017

Genichiro Soma

5

1 reference

3 August 2017

Hideki Kobara

7

1 reference

3 August 2017

Masakazu Kohno

9

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3 August 2017

Mitsuomi Hirashima

10

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3 August 2017

language of work or name

English

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publication date

9 April 2013

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3 August 2017

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3 August 2017

volume

8

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3 August 2017

issue

4

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3 August 2017

page(s)

e60807

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Creative Commons Attribution 4.0 International

3 August 2017

copyright license

start time

9 April 2013

1 reference

April 2022 Public Data File from Crossref

copyright status

copyrighted

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cites work

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7 July 2018

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Underexpression of TIM-3 and blunted galectin-9-induced apoptosis of CD4+ T cells in rheumatoid arthritis

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Oral administration of artemisinin analog SM934 ameliorates lupus syndromes in MRL/lpr mice by inhibiting Th1 and Th17 cell responses.

21 January 2018

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The Tim-3 ligand galectin-9 negatively regulates CD8+ alloreactive T cell and prolongs survival of skin graft

21 January 2018

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21 January 2018

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Galectin-9 suppresses Th17 cell development in an IL-2-dependent but Tim-3-independent manner

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12 December 2020

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12 December 2020

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12 December 2020

Galectin-9 ameliorates acute GVH disease through the induction of T-cell apoptosis

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Galectin-9 expands immunosuppressive macrophages to ameliorate T-cell-mediated lung inflammation

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Galectin-9 suppresses the generation of Th17, promotes the induction of regulatory T cells, and regulates experimental autoimmune arthritis

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10.1371/JOURNAL.PONE.0060807

Identifiers

DOI

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3 August 2017

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3 August 2017

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