Xcr1 + type 1 conventional dendritic cells are essential mediators for atherosclerosis progression Article Swipe
Tianhan Li
,
Liaoxun Lu
,
Juanjuan Qiu
,
Xin Dong
,
Le Yang
,
Kan He
,
Yanrong Gu
,
Binhui Zhou
,
Tingting Jia
,
Toby Lawrence
,
Marie Malissen
,
Guixue Wang
,
Rong Huang
,
Hui Wang
,
Bernard Malissen
,
Yinming Liang
,
Lichen Zhang
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1101/2025.05.23.655779
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1101/2025.05.23.655779
Background Atherosclerosis is characterized by lipid accumulation within plaques, leading to foam cell formation and an inflammatory response within the aortic lesions. Lipid disorders have been extensively investigated, however the cellular and molecular mechanisms that trigger the inflammatory response in atherosclerotic plaques remain far from being fully understood. Xcr1 + cDC1 cells are newly identified antigen-presenting cells in activating immune cells. However, the role of cDC1 cells in the development of atherosclerosis remains highly controversial. Results We first confirmed the presence of cDC1 within human atherosclerotic plaques and discovered a significant association between the increasing cDC1 numbers and atherosclerosis progression in mice. Subsequently, we established Xcr1 Cre-Gfp Rosa26 LSL-DTA ApoE −/− mice, a novel and complex genetic model, in which cDC1 was constitutively depleted in vivo during atherosclerosis development. Intriguingly, we observed a notable reduction in atherosclerotic lesions in hyperlipidemic mice, alongside suppressed T cell activation of both CD4 + and CD8 + subsets in the aortic plaques. Notably, aortic macrophages and serum lipid levels were not significantly changed in the cDC1-depleted mice. Single-cell RNA sequencing revealed heterogeneity of Xcr1 + cDC1 cells across the aorta and lymphoid organs under hyperlipidemic conditions. As Xcr1 is the sole receptor for Xcl1, we next explored to target Xcr1 + cDC1 cells via Xcl1 by establishing Xcl1 and ApoE deficient mice. Xcl1 knockout mice exhibited decreased atherosclerotic plaque formation and reduced aortic cDC1 accumulation, indicating that Xcl1 contributes to cDC1-mediated atherosclerotic lesion development. Conclusions Our results reveal crucial roles of cDC1 in atherosclerosis progression and provide insights into the development of immunotherapies by targeting cDC1 through Xcl1.
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- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1101/2025.05.23.655779
- https://www.biorxiv.org/content/biorxiv/early/2025/05/28/2025.05.23.655779.full.pdf
- OA Status
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- References
- 74
- Related Works
- 10
- OpenAlex ID
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Raw OpenAlex JSON
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- DOI
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https://doi.org/10.1101/2025.05.23.655779Digital Object Identifier
- Title
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Xcr1 + type 1 conventional dendritic cells are essential mediators for atherosclerosis progressionWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2025Year of publication
- Publication date
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2025-05-28Full publication date if available
- Authors
-
Tianhan Li, Liaoxun Lu, Juanjuan Qiu, Xin Dong, Le Yang, Kan He, Yanrong Gu, Binhui Zhou, Tingting Jia, Toby Lawrence, Marie Malissen, Guixue Wang, Rong Huang, Hui Wang, Bernard Malissen, Yinming Liang, Lichen ZhangList of authors in order
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https://doi.org/10.1101/2025.05.23.655779Publisher landing page
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https://www.biorxiv.org/content/biorxiv/early/2025/05/28/2025.05.23.655779.full.pdfDirect link to full text PDF
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YesWhether a free full text is available
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greenOpen access status per OpenAlex
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https://www.biorxiv.org/content/biorxiv/early/2025/05/28/2025.05.23.655779.full.pdfDirect OA link when available
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Type (biology), Biology, EcologyTop concepts (fields/topics) attached by OpenAlex
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.serum | 163 |
| abstract_inverted_index.under | 190 |
| abstract_inverted_index.which | 120 |
| abstract_inverted_index.Rosa26 | 108 |
| abstract_inverted_index.across | 184 |
| abstract_inverted_index.aortic | 21, 157, 160, 229 |
| abstract_inverted_index.cells. | 61 |
| abstract_inverted_index.during | 127 |
| abstract_inverted_index.highly | 74 |
| abstract_inverted_index.immune | 60 |
| abstract_inverted_index.lesion | 239 |
| abstract_inverted_index.levels | 165 |
| abstract_inverted_index.model, | 118 |
| abstract_inverted_index.organs | 189 |
| abstract_inverted_index.plaque | 225 |
| abstract_inverted_index.remain | 43 |
| abstract_inverted_index.reveal | 244 |
| abstract_inverted_index.target | 205 |
| abstract_inverted_index.within | 8, 19, 84 |
| abstract_inverted_index.Cre-Gfp | 107 |
| abstract_inverted_index.LSL-DTA | 109 |
| abstract_inverted_index.Results | 76 |
| abstract_inverted_index.between | 93 |
| abstract_inverted_index.changed | 169 |
| abstract_inverted_index.complex | 116 |
| abstract_inverted_index.crucial | 245 |
| abstract_inverted_index.genetic | 117 |
| abstract_inverted_index.however | 29 |
| abstract_inverted_index.leading | 10 |
| abstract_inverted_index.lesions | 138 |
| abstract_inverted_index.notable | 134 |
| abstract_inverted_index.numbers | 97 |
| abstract_inverted_index.plaques | 42, 87 |
| abstract_inverted_index.provide | 253 |
| abstract_inverted_index.reduced | 228 |
| abstract_inverted_index.remains | 73 |
| abstract_inverted_index.results | 243 |
| abstract_inverted_index.subsets | 154 |
| abstract_inverted_index.through | 263 |
| abstract_inverted_index.trigger | 36 |
| abstract_inverted_index.−/− | 111 |
| abstract_inverted_index.Abstract | 0 |
| abstract_inverted_index.However, | 62 |
| abstract_inverted_index.Notably, | 159 |
| abstract_inverted_index.cellular | 31 |
| abstract_inverted_index.depleted | 124 |
| abstract_inverted_index.explored | 203 |
| abstract_inverted_index.insights | 254 |
| abstract_inverted_index.knockout | 220 |
| abstract_inverted_index.lesions. | 22 |
| abstract_inverted_index.lymphoid | 188 |
| abstract_inverted_index.observed | 132 |
| abstract_inverted_index.plaques, | 9 |
| abstract_inverted_index.plaques. | 158 |
| abstract_inverted_index.presence | 81 |
| abstract_inverted_index.receptor | 198 |
| abstract_inverted_index.response | 18, 39 |
| abstract_inverted_index.revealed | 177 |
| abstract_inverted_index.alongside | 142 |
| abstract_inverted_index.confirmed | 79 |
| abstract_inverted_index.decreased | 223 |
| abstract_inverted_index.deficient | 217 |
| abstract_inverted_index.disorders | 24 |
| abstract_inverted_index.exhibited | 222 |
| abstract_inverted_index.formation | 14, 226 |
| abstract_inverted_index.molecular | 33 |
| abstract_inverted_index.reduction | 135 |
| abstract_inverted_index.targeting | 261 |
| abstract_inverted_index.Background | 1 |
| abstract_inverted_index.activating | 59 |
| abstract_inverted_index.activation | 146 |
| abstract_inverted_index.discovered | 89 |
| abstract_inverted_index.identified | 55 |
| abstract_inverted_index.increasing | 95 |
| abstract_inverted_index.indicating | 232 |
| abstract_inverted_index.mechanisms | 34 |
| abstract_inverted_index.sequencing | 176 |
| abstract_inverted_index.suppressed | 143 |
| abstract_inverted_index.Conclusions | 241 |
| abstract_inverted_index.Single-cell | 174 |
| abstract_inverted_index.association | 92 |
| abstract_inverted_index.conditions. | 192 |
| abstract_inverted_index.contributes | 235 |
| abstract_inverted_index.development | 70, 257 |
| abstract_inverted_index.established | 105 |
| abstract_inverted_index.extensively | 27 |
| abstract_inverted_index.macrophages | 161 |
| abstract_inverted_index.progression | 100, 251 |
| abstract_inverted_index.significant | 91 |
| abstract_inverted_index.understood. | 48 |
| abstract_inverted_index.accumulation | 7 |
| abstract_inverted_index.development. | 129, 240 |
| abstract_inverted_index.establishing | 213 |
| abstract_inverted_index.inflammatory | 17, 38 |
| abstract_inverted_index.Intriguingly, | 130 |
| abstract_inverted_index.Subsequently, | 103 |
| abstract_inverted_index.accumulation, | 231 |
| abstract_inverted_index.cDC1-depleted | 172 |
| abstract_inverted_index.cDC1-mediated | 237 |
| abstract_inverted_index.characterized | 4 |
| abstract_inverted_index.heterogeneity | 178 |
| abstract_inverted_index.investigated, | 28 |
| abstract_inverted_index.significantly | 168 |
| abstract_inverted_index.constitutively | 123 |
| abstract_inverted_index.controversial. | 75 |
| abstract_inverted_index.hyperlipidemic | 140, 191 |
| abstract_inverted_index.Atherosclerosis | 2 |
| abstract_inverted_index.atherosclerosis | 72, 99, 128, 250 |
| abstract_inverted_index.atherosclerotic | 41, 86, 137, 224, 238 |
| abstract_inverted_index.immunotherapies | 259 |
| abstract_inverted_index.antigen-presenting | 56 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 17 |
| citation_normalized_percentile.value | 0.21656607 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |