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TIM-4 Identifies Effector B Cells Expressing An IL-23-Driven Proinflammatory Cytokine Module That Promotes Immune Responses
B cells can express pro-inflammatory cytokines that promote a wide variety of immune responses. Here we show that B cells expressing the phosphatidylserine receptor TIM-4, preferentially express not only IL-17A, but also IL-22, IL-6, and GM-CSF - a collection of cytokines reminiscent of pathogenic T...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Cold Spring Harbor Laboratory
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10542535/ https://www.ncbi.nlm.nih.gov/pubmed/37790513 http://dx.doi.org/10.1101/2023.09.22.558524 |
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author | Ding, Qing Wu, Yufan Triglia, Elena Torlai Gommerman, Jennifer L. Subramanian, Ayshwarya Kuchroo, Vijay K. Rothstein, David M. |
author_facet | Ding, Qing Wu, Yufan Triglia, Elena Torlai Gommerman, Jennifer L. Subramanian, Ayshwarya Kuchroo, Vijay K. Rothstein, David M. |
author_sort | Ding, Qing |
collection | PubMed |
description | B cells can express pro-inflammatory cytokines that promote a wide variety of immune responses. Here we show that B cells expressing the phosphatidylserine receptor TIM-4, preferentially express not only IL-17A, but also IL-22, IL-6, and GM-CSF - a collection of cytokines reminiscent of pathogenic Th17 cells. Expression of this proinflammatory module requires B cell expression of IL-23R, RORγt and IL-17. IL-17 expressed by TIM-4(+) B cells not only enhances the severity of experimental autoimmune encephalomyelitis (EAE) and promotes allograft rejection, but also acts in an autocrine manner to prevent their conversion into IL-10-expressing B cells with regulatory function. Thus, IL-17 acts as an inflammatory mediator and also enforces the proinflammatory activity of TIM-4(+) B cells. TIM-4 serves as a broad marker for effector B cells (Beff) that will allow the study of the signals regulating their differentiation and expression of their effector molecules. |
format | Online Article Text |
id | pubmed-10542535 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Cold Spring Harbor Laboratory |
record_format | MEDLINE/PubMed |
spelling | pubmed-105425352023-10-03 TIM-4 Identifies Effector B Cells Expressing An IL-23-Driven Proinflammatory Cytokine Module That Promotes Immune Responses Ding, Qing Wu, Yufan Triglia, Elena Torlai Gommerman, Jennifer L. Subramanian, Ayshwarya Kuchroo, Vijay K. Rothstein, David M. bioRxiv Article B cells can express pro-inflammatory cytokines that promote a wide variety of immune responses. Here we show that B cells expressing the phosphatidylserine receptor TIM-4, preferentially express not only IL-17A, but also IL-22, IL-6, and GM-CSF - a collection of cytokines reminiscent of pathogenic Th17 cells. Expression of this proinflammatory module requires B cell expression of IL-23R, RORγt and IL-17. IL-17 expressed by TIM-4(+) B cells not only enhances the severity of experimental autoimmune encephalomyelitis (EAE) and promotes allograft rejection, but also acts in an autocrine manner to prevent their conversion into IL-10-expressing B cells with regulatory function. Thus, IL-17 acts as an inflammatory mediator and also enforces the proinflammatory activity of TIM-4(+) B cells. TIM-4 serves as a broad marker for effector B cells (Beff) that will allow the study of the signals regulating their differentiation and expression of their effector molecules. Cold Spring Harbor Laboratory 2023-09-23 /pmc/articles/PMC10542535/ /pubmed/37790513 http://dx.doi.org/10.1101/2023.09.22.558524 Text en https://creativecommons.org/licenses/by-nc-nd/4.0/This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which allows reusers to copy and distribute the material in any medium or format in unadapted form only, for noncommercial purposes only, and only so long as attribution is given to the creator. |
spellingShingle | Article Ding, Qing Wu, Yufan Triglia, Elena Torlai Gommerman, Jennifer L. Subramanian, Ayshwarya Kuchroo, Vijay K. Rothstein, David M. TIM-4 Identifies Effector B Cells Expressing An IL-23-Driven Proinflammatory Cytokine Module That Promotes Immune Responses |
title | TIM-4 Identifies Effector B Cells Expressing An IL-23-Driven Proinflammatory Cytokine Module That Promotes Immune Responses |
title_full | TIM-4 Identifies Effector B Cells Expressing An IL-23-Driven Proinflammatory Cytokine Module That Promotes Immune Responses |
title_fullStr | TIM-4 Identifies Effector B Cells Expressing An IL-23-Driven Proinflammatory Cytokine Module That Promotes Immune Responses |
title_full_unstemmed | TIM-4 Identifies Effector B Cells Expressing An IL-23-Driven Proinflammatory Cytokine Module That Promotes Immune Responses |
title_short | TIM-4 Identifies Effector B Cells Expressing An IL-23-Driven Proinflammatory Cytokine Module That Promotes Immune Responses |
title_sort | tim-4 identifies effector b cells expressing an il-23-driven proinflammatory cytokine module that promotes immune responses |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10542535/ https://www.ncbi.nlm.nih.gov/pubmed/37790513 http://dx.doi.org/10.1101/2023.09.22.558524 |
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