The balance between conventional and unconventional T follicular helper cells influences autoreactive B cell responses
Invariant natural killer T (iNKT) cells are activated by glycolipids presented on CD1d. When iNKT cells interact with and activate B cells, they can differentiate into iNKT follicular helper (iNKTfh) cells, and here, we investigate how this, in turn, regulates conventional T follicular helper (Tfh)...
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| Vydané v: | Cell reports (Cambridge) Ročník 44; číslo 5; s. 115602 |
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| Hlavní autori: | , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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United States
Elsevier Inc
27.05.2025
Elsevier |
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| ISSN: | 2211-1247, 2211-1247 |
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| Abstract | Invariant natural killer T (iNKT) cells are activated by glycolipids presented on CD1d. When iNKT cells interact with and activate B cells, they can differentiate into iNKT follicular helper (iNKTfh) cells, and here, we investigate how this, in turn, regulates conventional T follicular helper (Tfh) cells. This is done in an autoimmune model where antibodies are produced against self-antigens relevant to the autoimmune disease systemic lupus erythematosus (SLE). We find a balance between iNKTfh and Tfh cells that directs the B cell response and influences Tfh cell generation. This altered balance also affects the specificities and increases the autoantibody response. We also show that CD1d expression by B cells is essential for iNKTfh cell generation. In conclusion, our data shed light on how T cell help for B cells is divided between conventional and unconventional helper cell populations and how this has an impact on autoreactive B cell responses.
[Display omitted]
•Conventional and unconventional T follicular helper cells influence each other•Autoreactive B cell responses are enhanced by the activation of iNKTfh cells•Activation of iNKTfh cells is connected to interaction with CD1d expressed by B cells
In this study, He et al. find that there is a balance between conventional and unconventional T helper cells and that this influences autoreactive B cell responses. They find that when iNKTfh cells are activated, they limit the expansion of Tfh cells, but the resulting autoreactive B cell response is increased. |
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| AbstractList | Invariant natural killer T (iNKT) cells are activated by glycolipids presented on CD1d. When iNKT cells interact with and activate B cells, they can differentiate into iNKT follicular helper (iNKTfh) cells, and here, we investigate how this, in turn, regulates conventional T follicular helper (Tfh) cells. This is done in an autoimmune model where antibodies are produced against self-antigens relevant to the autoimmune disease systemic lupus erythematosus (SLE). We find a balance between iNKTfh and Tfh cells that directs the B cell response and influences Tfh cell generation. This altered balance also affects the specificities and increases the autoantibody response. We also show that CD1d expression by B cells is essential for iNKTfh cell generation. In conclusion, our data shed light on how T cell help for B cells is divided between conventional and unconventional helper cell populations and how this has an impact on autoreactive B cell responses. Invariant natural killer T (iNKT) cells are activated by glycolipids presented on CD1d. When iNKT cells interact with and activate B cells, they can differentiate into iNKT follicular helper (iNKTfh) cells, and here, we investigate how this, in turn, regulates conventional T follicular helper (Tfh) cells. This is done in an autoimmune model where antibodies are produced against self-antigens relevant to the autoimmune disease systemic lupus erythematosus (SLE). We find a balance between iNKTfh and Tfh cells that directs the B cell response and influences Tfh cell generation. This altered balance also affects the specificities and increases the autoantibody response. We also show that CD1d expression by B cells is essential for iNKTfh cell generation. In conclusion, our data shed light on how T cell help for B cells is divided between conventional and unconventional helper cell populations and how this has an impact on autoreactive B cell responses.Invariant natural killer T (iNKT) cells are activated by glycolipids presented on CD1d. When iNKT cells interact with and activate B cells, they can differentiate into iNKT follicular helper (iNKTfh) cells, and here, we investigate how this, in turn, regulates conventional T follicular helper (Tfh) cells. This is done in an autoimmune model where antibodies are produced against self-antigens relevant to the autoimmune disease systemic lupus erythematosus (SLE). We find a balance between iNKTfh and Tfh cells that directs the B cell response and influences Tfh cell generation. This altered balance also affects the specificities and increases the autoantibody response. We also show that CD1d expression by B cells is essential for iNKTfh cell generation. In conclusion, our data shed light on how T cell help for B cells is divided between conventional and unconventional helper cell populations and how this has an impact on autoreactive B cell responses. Invariant natural killer T (iNKT) cells are activated by glycolipids presented on CD1d. When iNKT cells interact with and activate B cells, they can differentiate into iNKT follicular helper (iNKTfh) cells, and here, we investigate how this, in turn, regulates conventional T follicular helper (Tfh) cells. This is done in an autoimmune model where antibodies are produced against self-antigens relevant to the autoimmune disease systemic lupus erythematosus (SLE). We find a balance between iNKTfh and Tfh cells that directs the B cell response and influences Tfh cell generation. This altered balance also affects the specificities and increases the autoantibody response. We also show that CD1d expression by B cells is essential for iNKTfh cell generation. In conclusion, our data shed light on how T cell help for B cells is divided between conventional and unconventional helper cell populations and how this has an impact on autoreactive B cell responses. Invariant natural killer T (iNKT) cells are activated by glycolipids presented on CD1d. When iNKT cells interact with and activate B cells, they can differentiate into iNKT follicular helper (iNKTfh) cells, and here, we investigate how this, in turn, regulates conventional T follicular helper (Tfh) cells. This is done in an autoimmune model where antibodies are produced against self-antigens relevant to the autoimmune disease systemic lupus erythematosus (SLE). We find a balance between iNKTfh and Tfh cells that directs the B cell response and influences Tfh cell generation. This altered balance also affects the specificities and increases the autoantibody response. We also show that CD1d expression by B cells is essential for iNKTfh cell generation. In conclusion, our data shed light on how T cell help for B cells is divided between conventional and unconventional helper cell populations and how this has an impact on autoreactive B cell responses. [Display omitted] •Conventional and unconventional T follicular helper cells influence each other•Autoreactive B cell responses are enhanced by the activation of iNKTfh cells•Activation of iNKTfh cells is connected to interaction with CD1d expressed by B cells In this study, He et al. find that there is a balance between conventional and unconventional T helper cells and that this influences autoreactive B cell responses. They find that when iNKTfh cells are activated, they limit the expansion of Tfh cells, but the resulting autoreactive B cell response is increased. |
| ArticleNumber | 115602 |
| Author | Ramiro, Almudena R. Li, Quan-Zhen Barral, Patricia Moreews, Marion Cai, Curtis Gaya, Mauro Batista, Facundo D. Karlsson, Mikael C.I. Chen, Guangchun Del Monte Monge, Alberto Buggert, Marcus Pei, Shengduo He, Chenfei Wang, Shan |
| Author_xml | – sequence: 1 givenname: Chenfei surname: He fullname: He, Chenfei organization: Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Tomtebodavägen 16, Solna Campus, 171 65 Stockholm, Sweden – sequence: 2 givenname: Shan surname: Wang fullname: Wang, Shan organization: Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Tomtebodavägen 16, Solna Campus, 171 65 Stockholm, Sweden – sequence: 3 givenname: Marion surname: Moreews fullname: Moreews, Marion organization: Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Tomtebodavägen 16, Solna Campus, 171 65 Stockholm, Sweden – sequence: 4 givenname: Shengduo surname: Pei fullname: Pei, Shengduo organization: Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Tomtebodavägen 16, Solna Campus, 171 65 Stockholm, Sweden – sequence: 5 givenname: Guangchun surname: Chen fullname: Chen, Guangchun organization: Microarray Core, Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA – sequence: 6 givenname: Quan-Zhen surname: Li fullname: Li, Quan-Zhen organization: Microarray Core, Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA – sequence: 7 givenname: Alberto surname: Del Monte Monge fullname: Del Monte Monge, Alberto organization: Spanish Center for Cardiovascular Research, Melchor Fernandez Almagro 3, Madrid, Spain – sequence: 8 givenname: Almudena R. surname: Ramiro fullname: Ramiro, Almudena R. organization: Spanish Center for Cardiovascular Research, Melchor Fernandez Almagro 3, Madrid, Spain – sequence: 9 givenname: Curtis surname: Cai fullname: Cai, Curtis organization: Center for Infections Medicine, Department of Medicine Karolinska Institutet, Huddinge, Sweden – sequence: 10 givenname: Mauro surname: Gaya fullname: Gaya, Mauro organization: Centre d'Immunologie de Marseille-Luminy (CIML), Aix Marseille Université, INSERM, CNRS, Marseille, France – sequence: 11 givenname: Patricia surname: Barral fullname: Barral, Patricia organization: The Francis Crick Institute, London, UK – sequence: 12 givenname: Marcus surname: Buggert fullname: Buggert, Marcus organization: Center for Infections Medicine, Department of Medicine Karolinska Institutet, Huddinge, Sweden – sequence: 13 givenname: Facundo D. surname: Batista fullname: Batista, Facundo D. organization: Ragon Institute of MGH, MIT, and Harvard, 400 Technology Square, Cambridge, MA 02139, USA – sequence: 14 givenname: Mikael C.I. orcidid: 0000-0001-5582-614X surname: Karlsson fullname: Karlsson, Mikael C.I. email: mikael.karlsson@ki.se organization: Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Tomtebodavägen 16, Solna Campus, 171 65 Stockholm, Sweden |
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| Keywords | CP: Immunology CD1d germinal center apoptotic cells autoimmune disease T follicular helper cells |
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| SubjectTerms | Animals Antigens, CD1d - immunology Antigens, CD1d - metabolism apoptotic cells Autoantibodies - immunology autoimmune disease Autoimmunity B-Lymphocytes - immunology CD1d Cell Differentiation CP: Immunology germinal center Lupus Erythematosus, Systemic - immunology Lymphocyte Activation - immunology Mice Mice, Inbred C57BL Natural Killer T-Cells - immunology T follicular helper cells T Follicular Helper Cells - immunology T-Lymphocytes, Helper-Inducer - immunology |
| Title | The balance between conventional and unconventional T follicular helper cells influences autoreactive B cell responses |
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