Tim-3 signaling blockade with α-lactose induces compensatory TIGIT expression in Plasmodium berghei ANKA-infected mice
Identifieur interne : 000B92 ( Ncbi/Checkpoint ); précédent : 000B91; suivant : 000B93Tim-3 signaling blockade with α-lactose induces compensatory TIGIT expression in Plasmodium berghei ANKA-infected mice
Auteurs : Yiwei Zhang [République populaire de Chine] ; Ning Jiang [République populaire de Chine] ; Ting Zhang [République populaire de Chine] ; Ran Chen [République populaire de Chine] ; Ying Feng [République populaire de Chine] ; Xiaoyu Sang [République populaire de Chine] ; Na Yang [République populaire de Chine] ; Qijun Chen [République populaire de Chine]Source :
- Parasites & Vectors [ 1756-3305 ] ; 2019.
Abstract
Malaria, one of the largest health burdens worldwide, is caused by
Tim-3 expression on critical lymphocyte populations and the proportion of these cells, as well as the levels of cytokines in the sera of infected mice, were detected by flow cytometry. Further,
Increased Tim-3 expression on splenic CD8+ and splenic CD4+, and circulatory CD4+ T cells was associated with a reduction in the proportion of these cells. Furthermore, the levels of interleukin (IL)-2, IL-4, IL-6, IL-22, and interferon (IFN)-γ, but not that of tumor necrosis factor alpha (TNF-α), IL-10, and IL-9, increased to their highest levels at day 4 post-infection and decreased thereafter. Blocking Tim-3 signaling
Tim-3 on lymphocytes negatively regulates cell-mediated immunity against
Url:
DOI: 10.1186/s13071-019-3788-x
PubMed: 31711531
PubMed Central: 6849286
Affiliations:
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ANKA-infected mice</title>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Tim-3 signaling blockade with α-lactose induces compensatory TIGIT expression in <italic>Plasmodium berghei</italic>
ANKA-infected mice</title>
<author><name sortKey="Zhang, Yiwei" sort="Zhang, Yiwei" uniqKey="Zhang Y" first="Yiwei" last="Zhang">Yiwei Zhang</name>
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Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
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Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>The Research Unit for Pathogenic Mechanisms of Zoonotic Parasites, Chinese Academy of Medical Sciences, 120 Dongling Road, Shenyang</wicri:regionArea>
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Shenyang, 110866 China</nlm:aff>
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<author><name sortKey="Chen, Ran" sort="Chen, Ran" uniqKey="Chen R" first="Ran" last="Chen">Ran Chen</name>
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<institution-id institution-id-type="GRID">grid.412557.0</institution-id>
<institution>Key Laboratory of Livestock Infectious Diseases in Northeast China, Ministry of Education, College of Animal Science and Veterinary Medicine,</institution>
<institution>Shenyang Agricultural University,</institution>
</institution-wrap>
Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shenyang</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="Aff2">The Research Unit for Pathogenic Mechanisms of Zoonotic Parasites, Chinese Academy of Medical Sciences, 120 Dongling Road, Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>The Research Unit for Pathogenic Mechanisms of Zoonotic Parasites, Chinese Academy of Medical Sciences, 120 Dongling Road, Shenyang</wicri:regionArea>
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<author><name sortKey="Feng, Ying" sort="Feng, Ying" uniqKey="Feng Y" first="Ying" last="Feng">Ying Feng</name>
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Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shenyang</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="Aff2">The Research Unit for Pathogenic Mechanisms of Zoonotic Parasites, Chinese Academy of Medical Sciences, 120 Dongling Road, Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>The Research Unit for Pathogenic Mechanisms of Zoonotic Parasites, Chinese Academy of Medical Sciences, 120 Dongling Road, Shenyang</wicri:regionArea>
<wicri:noRegion>Shenyang</wicri:noRegion>
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<author><name sortKey="Sang, Xiaoyu" sort="Sang, Xiaoyu" uniqKey="Sang X" first="Xiaoyu" last="Sang">Xiaoyu Sang</name>
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Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shenyang</wicri:regionArea>
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<affiliation wicri:level="1"><nlm:aff id="Aff2">The Research Unit for Pathogenic Mechanisms of Zoonotic Parasites, Chinese Academy of Medical Sciences, 120 Dongling Road, Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>The Research Unit for Pathogenic Mechanisms of Zoonotic Parasites, Chinese Academy of Medical Sciences, 120 Dongling Road, Shenyang</wicri:regionArea>
<wicri:noRegion>Shenyang</wicri:noRegion>
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<author><name sortKey="Yang, Na" sort="Yang, Na" uniqKey="Yang N" first="Na" last="Yang">Na Yang</name>
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<institution>Shenyang Agricultural University,</institution>
</institution-wrap>
Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shenyang</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="Aff2">The Research Unit for Pathogenic Mechanisms of Zoonotic Parasites, Chinese Academy of Medical Sciences, 120 Dongling Road, Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>The Research Unit for Pathogenic Mechanisms of Zoonotic Parasites, Chinese Academy of Medical Sciences, 120 Dongling Road, Shenyang</wicri:regionArea>
<wicri:noRegion>Shenyang</wicri:noRegion>
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<author><name sortKey="Chen, Qijun" sort="Chen, Qijun" uniqKey="Chen Q" first="Qijun" last="Chen">Qijun Chen</name>
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<institution>Key Laboratory of Livestock Infectious Diseases in Northeast China, Ministry of Education, College of Animal Science and Veterinary Medicine,</institution>
<institution>Shenyang Agricultural University,</institution>
</institution-wrap>
Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shenyang</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="Aff2">The Research Unit for Pathogenic Mechanisms of Zoonotic Parasites, Chinese Academy of Medical Sciences, 120 Dongling Road, Shenyang, 110866 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>The Research Unit for Pathogenic Mechanisms of Zoonotic Parasites, Chinese Academy of Medical Sciences, 120 Dongling Road, Shenyang</wicri:regionArea>
<wicri:noRegion>Shenyang</wicri:noRegion>
</affiliation>
</author>
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<series><title level="j">Parasites & Vectors</title>
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<imprint><date when="2019">2019</date>
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p id="Par1">Malaria, one of the largest health burdens worldwide, is caused by <italic>Plasmodium</italic>
spp. infection. Upon infection, the host’s immune system begins to clear the parasites. However, <italic>Plasmodium</italic>
species have evolved to escape the host’s immune clearance. T-cell immunoglobulin and mucin domain 3 (Tim-3), a surface molecule on most immune cells, is often referred to as an exhaustion marker. Galectin (Gal)-9 is a Tim-3 ligand and the T helper (Th) 1 cell response is inhibited when Gal-9 binds to Tim-3. In the present study, dynamic expression of Tim-3 on key populations of lymphocytes during infection periods of <italic>Plasmodium berghei</italic>
and its significance in disease resistance and pathogenesis were explored.</p>
</sec>
<sec><title>Methods</title>
<p id="Par2">Tim-3 expression on critical lymphocyte populations and the proportion of these cells, as well as the levels of cytokines in the sera of infected mice, were detected by flow cytometry. Further, <italic>in vitro</italic>
anti-Tim-3 assay using an anti-Tim-3 antibody and <italic>in vivo</italic>
Tim-3-Gal-9 signaling blockade assays using α-lactose (an antagonist of Gal-9) were conducted. An Annexin V Apoptosis Detection Kit with propidium iodide was used to detect apoptosis. In addition, proteins associated with apoptosis in lung and spleen tissues were confirmed by Western blotting assays.</p>
</sec>
<sec><title>Results</title>
<p id="Par3">Increased Tim-3 expression on splenic CD8<sup>+</sup>
and splenic CD4<sup>+</sup>
, and circulatory CD4<sup>+</sup>
T cells was associated with a reduction in the proportion of these cells. Furthermore, the levels of interleukin (IL)-2, IL-4, IL-6, IL-22, and interferon (IFN)-γ, but not that of tumor necrosis factor alpha (TNF-α), IL-10, and IL-9, increased to their highest levels at day 4 post-infection and decreased thereafter. Blocking Tim-3 signaling <italic>in vitro</italic>
inhibited lymphocyte apoptosis. Tim-3-Gal-9 signaling blockade <italic>in vivo</italic>
did not protect the mice, but induced the expression of the immunosuppressive molecule, T cell immunoreceptor with Ig and ITIM domains (TIGIT), in <italic>Plasmodium berghei</italic>
ANKA<italic>-</italic>
infected mice.</p>
</sec>
<sec><title>Conclusions</title>
<p id="Par4">Tim-3 on lymphocytes negatively regulates cell-mediated immunity against <italic>Plasmodium</italic>
infection, and blocking Tim-3-galectin 9 signaling using α-lactose did not significantly protect the mice; however, it induced the compensatory expression of TIGIT. Further investigations are required to identify whether combined blockade of Tim-3 and TIGIT signaling could achieve a better protective effect.<graphic position="anchor" xlink:href="13071_2019_3788_Figa_HTML" id="MO100"></graphic>
</p>
</sec>
</div>
</front>
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</div1>
</back>
</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Yiwei" sort="Zhang, Yiwei" uniqKey="Zhang Y" first="Yiwei" last="Zhang">Yiwei Zhang</name>
</noRegion>
<name sortKey="Chen, Qijun" sort="Chen, Qijun" uniqKey="Chen Q" first="Qijun" last="Chen">Qijun Chen</name>
<name sortKey="Chen, Qijun" sort="Chen, Qijun" uniqKey="Chen Q" first="Qijun" last="Chen">Qijun Chen</name>
<name sortKey="Chen, Ran" sort="Chen, Ran" uniqKey="Chen R" first="Ran" last="Chen">Ran Chen</name>
<name sortKey="Chen, Ran" sort="Chen, Ran" uniqKey="Chen R" first="Ran" last="Chen">Ran Chen</name>
<name sortKey="Feng, Ying" sort="Feng, Ying" uniqKey="Feng Y" first="Ying" last="Feng">Ying Feng</name>
<name sortKey="Feng, Ying" sort="Feng, Ying" uniqKey="Feng Y" first="Ying" last="Feng">Ying Feng</name>
<name sortKey="Jiang, Ning" sort="Jiang, Ning" uniqKey="Jiang N" first="Ning" last="Jiang">Ning Jiang</name>
<name sortKey="Jiang, Ning" sort="Jiang, Ning" uniqKey="Jiang N" first="Ning" last="Jiang">Ning Jiang</name>
<name sortKey="Sang, Xiaoyu" sort="Sang, Xiaoyu" uniqKey="Sang X" first="Xiaoyu" last="Sang">Xiaoyu Sang</name>
<name sortKey="Sang, Xiaoyu" sort="Sang, Xiaoyu" uniqKey="Sang X" first="Xiaoyu" last="Sang">Xiaoyu Sang</name>
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<name sortKey="Zhang, Yiwei" sort="Zhang, Yiwei" uniqKey="Zhang Y" first="Yiwei" last="Zhang">Yiwei Zhang</name>
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</tree>
</affiliations>
</record>
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