Humanized CXCL12 antibody delays onset and modulates immune response in alopecia areata mice: insights from single-cell RNA sequencing

It has been demonstrated that CXCL12 inhibits hair growth via CXCR4, and its neutralizing antibody (Ab) increases hair growth in alopecia areata (AA). However, the molecular mechanisms have not been fully elucidated. In the present study, we further prepared humanized CXCL12 Ab for AA treatment and...

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Main Authors: Seungchan An, Mei Zheng, In Guk Park, Sang Gyu Park, Minsoo Noh, Jong-Hyuk Sung
Format: Article
Language:English
Published: Frontiers Media S.A. 2024-10-01
Series:Frontiers in Immunology
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Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2024.1444777/full
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author Seungchan An
Mei Zheng
In Guk Park
Sang Gyu Park
Minsoo Noh
Jong-Hyuk Sung
author_facet Seungchan An
Mei Zheng
In Guk Park
Sang Gyu Park
Minsoo Noh
Jong-Hyuk Sung
author_sort Seungchan An
collection DOAJ
description It has been demonstrated that CXCL12 inhibits hair growth via CXCR4, and its neutralizing antibody (Ab) increases hair growth in alopecia areata (AA). However, the molecular mechanisms have not been fully elucidated. In the present study, we further prepared humanized CXCL12 Ab for AA treatment and investigated underlying molecular mechanisms using single-cell RNA sequencing. Subcutaneous injection of humanized CXCL12 Ab significantly delayed AA onset in mice, and dorsal skin was analyzed. T cells and dendritic cells/macrophages were increased in the AA model, but decreased after CXCL12 Ab treatment. Pseudobulk RNA sequencing identified 153 differentially expressed genes that were upregulated in AA model and downregulated after Ab treatment. Gene ontology analysis revealed that immune cell chemotaxis and cellular response to type II interferon were upregulated in AA model but downregulated after Ab treatment. We further identified key immune cell-related genes such as Ifng, Cd8a, Ccr5, Ccl4, Ccl5, and Il21r, which were colocalized with Cxcr4 in T cells and regulated by CXCL12 Ab treatment. Notably, CD8+ T cells were significantly increased and activated via Jak/Stat pathway in the AA model but inactivated after CXCL12 Ab treatment. Collectively, these results indicate that humanized CXCL12 Ab is promising for AA treatment via immune modulatory effects.
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issn 1664-3224
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spelling doaj-art-9e5645b04b124fde84cf73effb22dc762025-08-20T02:17:02ZengFrontiers Media S.A.Frontiers in Immunology1664-32242024-10-011510.3389/fimmu.2024.14447771444777Humanized CXCL12 antibody delays onset and modulates immune response in alopecia areata mice: insights from single-cell RNA sequencingSeungchan An0Mei Zheng1In Guk Park2Sang Gyu Park3Minsoo Noh4Jong-Hyuk Sung5College of Pharmacy, Natural Products Research Institute, Seoul National University, Seoul, Republic of KoreaEpi Biotech Co., Ltd., R&D Center, Incheon, Republic of KoreaCollege of Pharmacy, Natural Products Research Institute, Seoul National University, Seoul, Republic of KoreaCollege of Pharmacy, Ajou University, Suwon, Republic of KoreaCollege of Pharmacy, Natural Products Research Institute, Seoul National University, Seoul, Republic of KoreaEpi Biotech Co., Ltd., R&D Center, Incheon, Republic of KoreaIt has been demonstrated that CXCL12 inhibits hair growth via CXCR4, and its neutralizing antibody (Ab) increases hair growth in alopecia areata (AA). However, the molecular mechanisms have not been fully elucidated. In the present study, we further prepared humanized CXCL12 Ab for AA treatment and investigated underlying molecular mechanisms using single-cell RNA sequencing. Subcutaneous injection of humanized CXCL12 Ab significantly delayed AA onset in mice, and dorsal skin was analyzed. T cells and dendritic cells/macrophages were increased in the AA model, but decreased after CXCL12 Ab treatment. Pseudobulk RNA sequencing identified 153 differentially expressed genes that were upregulated in AA model and downregulated after Ab treatment. Gene ontology analysis revealed that immune cell chemotaxis and cellular response to type II interferon were upregulated in AA model but downregulated after Ab treatment. We further identified key immune cell-related genes such as Ifng, Cd8a, Ccr5, Ccl4, Ccl5, and Il21r, which were colocalized with Cxcr4 in T cells and regulated by CXCL12 Ab treatment. Notably, CD8+ T cells were significantly increased and activated via Jak/Stat pathway in the AA model but inactivated after CXCL12 Ab treatment. Collectively, these results indicate that humanized CXCL12 Ab is promising for AA treatment via immune modulatory effects.https://www.frontiersin.org/articles/10.3389/fimmu.2024.1444777/fullCXCL12humanized antibodyalopecia areataCD8 + T cellinterferon-gamma
spellingShingle Seungchan An
Mei Zheng
In Guk Park
Sang Gyu Park
Minsoo Noh
Jong-Hyuk Sung
Humanized CXCL12 antibody delays onset and modulates immune response in alopecia areata mice: insights from single-cell RNA sequencing
Frontiers in Immunology
CXCL12
humanized antibody
alopecia areata
CD8 + T cell
interferon-gamma
title Humanized CXCL12 antibody delays onset and modulates immune response in alopecia areata mice: insights from single-cell RNA sequencing
title_full Humanized CXCL12 antibody delays onset and modulates immune response in alopecia areata mice: insights from single-cell RNA sequencing
title_fullStr Humanized CXCL12 antibody delays onset and modulates immune response in alopecia areata mice: insights from single-cell RNA sequencing
title_full_unstemmed Humanized CXCL12 antibody delays onset and modulates immune response in alopecia areata mice: insights from single-cell RNA sequencing
title_short Humanized CXCL12 antibody delays onset and modulates immune response in alopecia areata mice: insights from single-cell RNA sequencing
title_sort humanized cxcl12 antibody delays onset and modulates immune response in alopecia areata mice insights from single cell rna sequencing
topic CXCL12
humanized antibody
alopecia areata
CD8 + T cell
interferon-gamma
url https://www.frontiersin.org/articles/10.3389/fimmu.2024.1444777/full
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