NLRX1 Regulates Effector and Metabolic Functions of CD4+ T Cells Article Swipe
Andrew Leber
,
Raquel Hontecillas
,
Nuria Tubau‐Juni
,
Victoria Zoccoli-Rodriguez
,
Matthew W. Hulver
,
Ryan P. McMillan
,
Kristin Eden
,
Irving C. Allen
,
Josep Bassaganya-Riera
·
YOU?
·
· 2017
· Open Access
·
· DOI: https://doi.org/10.4049/jimmunol.1601547
YOU?
·
· 2017
· Open Access
·
· DOI: https://doi.org/10.4049/jimmunol.1601547
Nucleotide oligomerization domain–like receptor X1 (NLRX1) has been implicated in viral response, cancer progression, and inflammatory disorders; however, its role as a dual modulator of CD4+ T cell function and metabolism has not been defined. The loss of NLRX1 results in increased disease severity, populations of Th1 and Th17 cells, and inflammatory markers (IFN-γ, TNF-α, and IL-17) in mice with dextran sodium sulfate–induced colitis. To further characterize this phenotype, we used in vitro CD4+ T cell–differentiation assays and show that NLRX1-deficient T cells have a greater ability to differentiate into an inflammatory phenotype and possess greater proliferation rates. Further, NLRX1−/− cells have a decreased responsiveness to immune checkpoint pathways and greater rates of lactate dehydrogenase activity. When metabolic effects of the knockout are impaired, NLRX1-deficient cells do not display significant differences in differentiation or proliferation. To confirm the role of NLRX1 specifically in T cells, we used an adoptive-transfer model of colitis. Rag2−/− mice receiving NLRX1−/− naive or effector T cells experienced increased disease activity and effector T cell populations, whereas no differences were observed between groups receiving wild-type or NLRX1−/− regulatory T cells. Metabolic effects of NLRX1 deficiency are observed in a CD4-specific knockout of NLRX1 within a Citrobacter rodentium model of colitis. The aerobic glycolytic preference in NLRX1−/− effector T cells is combined with a decreased sensitivity to immunosuppressive checkpoint pathways to provide greater proliferative capabilities and an inflammatory phenotype bias leading to increased disease severity.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.4049/jimmunol.1601547
- https://www.jimmunol.org/content/jimmunol/198/6/2260.full.pdf
- OA Status
- bronze
- Cited By
- 47
- References
- 55
- Related Works
- 10
- OpenAlex ID
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All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W2586076311Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.4049/jimmunol.1601547Digital Object Identifier
- Title
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NLRX1 Regulates Effector and Metabolic Functions of CD4+ T CellsWork title
- Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2017Year of publication
- Publication date
-
2017-02-04Full publication date if available
- Authors
-
Andrew Leber, Raquel Hontecillas, Nuria Tubau‐Juni, Victoria Zoccoli-Rodriguez, Matthew W. Hulver, Ryan P. McMillan, Kristin Eden, Irving C. Allen, Josep Bassaganya-RieraList of authors in order
- Landing page
-
https://doi.org/10.4049/jimmunol.1601547Publisher landing page
- PDF URL
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https://www.jimmunol.org/content/jimmunol/198/6/2260.full.pdfDirect link to full text PDF
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YesWhether a free full text is available
- OA status
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bronzeOpen access status per OpenAlex
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https://www.jimmunol.org/content/jimmunol/198/6/2260.full.pdfDirect OA link when available
- Concepts
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Effector, Cell biology, BiologyTop concepts (fields/topics) attached by OpenAlex
- Cited by
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47Total citation count in OpenAlex
- Citations by year (recent)
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2025: 3, 2024: 2, 2023: 8, 2022: 5, 2021: 6Per-year citation counts (last 5 years)
- References (count)
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55Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.effects | 119, 186 |
| abstract_inverted_index.further | 66 |
| abstract_inverted_index.greater | 86, 96, 111, 226 |
| abstract_inverted_index.lactate | 114 |
| abstract_inverted_index.leading | 234 |
| abstract_inverted_index.markers | 53 |
| abstract_inverted_index.possess | 95 |
| abstract_inverted_index.provide | 225 |
| abstract_inverted_index.results | 40 |
| abstract_inverted_index.whereas | 171 |
| abstract_inverted_index.(IFN-γ, | 54 |
| abstract_inverted_index.Abstract | 0 |
| abstract_inverted_index.Further, | 99 |
| abstract_inverted_index.activity | 165 |
| abstract_inverted_index.colitis. | 64, 152, 204 |
| abstract_inverted_index.combined | 215 |
| abstract_inverted_index.defined. | 35 |
| abstract_inverted_index.effector | 159, 167, 211 |
| abstract_inverted_index.function | 29 |
| abstract_inverted_index.however, | 18 |
| abstract_inverted_index.knockout | 122, 195 |
| abstract_inverted_index.observed | 175, 191 |
| abstract_inverted_index.pathways | 109, 223 |
| abstract_inverted_index.receptor | 4 |
| abstract_inverted_index.Metabolic | 185 |
| abstract_inverted_index.activity. | 116 |
| abstract_inverted_index.decreased | 104, 218 |
| abstract_inverted_index.impaired, | 124 |
| abstract_inverted_index.increased | 42, 163, 236 |
| abstract_inverted_index.metabolic | 118 |
| abstract_inverted_index.modulator | 24 |
| abstract_inverted_index.phenotype | 93, 232 |
| abstract_inverted_index.receiving | 155, 178 |
| abstract_inverted_index.response, | 12 |
| abstract_inverted_index.rodentium | 201 |
| abstract_inverted_index.severity, | 44 |
| abstract_inverted_index.severity. | 238 |
| abstract_inverted_index.wild-type | 179 |
| abstract_inverted_index.Nucleotide | 1 |
| abstract_inverted_index.checkpoint | 108, 222 |
| abstract_inverted_index.deficiency | 189 |
| abstract_inverted_index.disorders; | 17 |
| abstract_inverted_index.glycolytic | 207 |
| abstract_inverted_index.implicated | 9 |
| abstract_inverted_index.metabolism | 31 |
| abstract_inverted_index.phenotype, | 69 |
| abstract_inverted_index.preference | 208 |
| abstract_inverted_index.regulatory | 182 |
| abstract_inverted_index.Citrobacter | 200 |
| abstract_inverted_index.Rag2−/− | 153 |
| abstract_inverted_index.differences | 131, 173 |
| abstract_inverted_index.experienced | 162 |
| abstract_inverted_index.populations | 45 |
| abstract_inverted_index.sensitivity | 219 |
| abstract_inverted_index.significant | 130 |
| abstract_inverted_index.CD4-specific | 194 |
| abstract_inverted_index.NLRX1−/− | 100, 156, 181, 210 |
| abstract_inverted_index.capabilities | 228 |
| abstract_inverted_index.characterize | 67 |
| abstract_inverted_index.inflammatory | 16, 52, 92, 231 |
| abstract_inverted_index.populations, | 170 |
| abstract_inverted_index.progression, | 14 |
| abstract_inverted_index.specifically | 142 |
| abstract_inverted_index.dehydrogenase | 115 |
| abstract_inverted_index.differentiate | 89 |
| abstract_inverted_index.domain–like | 3 |
| abstract_inverted_index.proliferation | 97 |
| abstract_inverted_index.proliferative | 227 |
| abstract_inverted_index.proliferation. | 135 |
| abstract_inverted_index.responsiveness | 105 |
| abstract_inverted_index.NLRX1-deficient | 81, 125 |
| abstract_inverted_index.differentiation | 133 |
| abstract_inverted_index.oligomerization | 2 |
| abstract_inverted_index.adoptive-transfer | 149 |
| abstract_inverted_index.immunosuppressive | 221 |
| abstract_inverted_index.sulfate–induced | 63 |
| abstract_inverted_index.cell–differentiation | 76 |
| cited_by_percentile_year.max | 99 |
| cited_by_percentile_year.min | 94 |
| corresponding_author_ids | https://openalex.org/A5101801206 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 9 |
| corresponding_institution_ids | https://openalex.org/I4210151352, https://openalex.org/I859038795 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.7900000214576721 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.89333516 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |