Single-cell RNA sequencing of submandibular gland reveals collagen type XV-positive fibroblasts as a disease-characterizing cell population of IgG4-related disease.

Collagen type XV Fibroblasts IgG4-related disease Single-cell RNA sequence

Journal

Arthritis research & therapy
ISSN: 1478-6362
Titre abrégé: Arthritis Res Ther
Pays: England
ID NLM: 101154438

Informations de publication

Date de publication:
20 Feb 2024
Historique:
received: 30 11 2023
accepted: 16 02 2024
medline: 21 2 2024
pubmed: 21 2 2024
entrez: 20 2 2024
Statut: epublish

Résumé

IgG4-related disease (IgG4-RD) is a systemic autoimmune disease with an unknown etiology, affecting single/multiple organ(s). Pathological findings include the infiltration of IgG4-producing plasma cells, obliterative phlebitis, and storiform fibrosis. Although immunological studies have shed light on the dysregulation of lymphocytes in IgG4-RD pathogenesis, the role of non-immune cells remains unclear. This study aimed to investigate the demographics and characteristics of non-immune cells in IgG4-RD and explore potential biomarkers derived from non-immune cells in the sera. We conducted single-cell RNA sequence (scRNA-seq) on non-immune cells isolated from submandibular glands of IgG4-RD patients. We focused on fibroblasts expressing collagen type XV and confirmed the presence of those fibroblasts using immunohistochemistry. Additionally, we measured the levels of collagen type XV in the sera of IgG4-RD patients. The scRNA-seq analysis revealed several distinct clusters consisting of fibroblasts, endothelial cells, ductal cells, and muscle cells. Differential gene expression analysis showed upregulation of COL15A1 in IgG4-RD fibroblasts compared to control subjects. Notably, COL15A1-positive fibroblasts exhibited a distinct transcriptome compared to COL15A1-negative counterparts. Immunohistochemical analysis confirmed a significant presence of collagen type XV-positive fibroblasts in IgG4-RD patients. Furthermore, immune-suppressive therapy in active IgG4-RD patients resulted in decreased serum levels of collagen type XV. Our findings suggest that collagen type XV-producing fibroblasts may represent a disease-characterizing non-immune cell population in IgG4-RD and hold potential as a disease-monitoring marker.

Identifiants

pubmed: 38378635
doi: 10.1186/s13075-024-03289-7
pii: 10.1186/s13075-024-03289-7
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

55

Subventions

Organisme : Japan Society for the Promotion of Science
ID : 21K08436

Informations de copyright

© 2024. The Author(s).

Références

Stone JH, Zen Y, Deshpande V. IgG4-related disease. N Engl J Med. 2012;366(6):539–51.
doi: 10.1056/NEJMra1104650 pubmed: 22316447
Mattoo H, Mahajan VS, Della-Torre E, Sekigami Y, Carruthers M, Wallace ZS, Deshpande V, Stone JH, Pillai S. De novo oligoclonal expansions of circulating plasmablasts in active and relapsing IgG4-related disease. J Allergy Clin Immunol. 2014;134(3):679–87.
doi: 10.1016/j.jaci.2014.03.034 pubmed: 24815737 pmcid: 4149918
Maehara T, Mattoo H, Mahajan VS, Murphy SJ, Yuen GJ, Ishiguro N, Ohta M, Moriyama M, Saeki T, Yamamoto H et al. The expansion in lymphoid organs of IL-4(+) BATF(+) T follicular helper cells is linked to IgG4 class switching in vivo. Life Sci Alliance 2018, 1(1).
Della-Torre E, Feeney E, Deshpande V, Mattoo H, Mahajan V, Kulikova M, Wallace ZS, Carruthers M, Chung RT, Pillai S, et al. B-cell depletion attenuates serological biomarkers of fibrosis and myofibroblast activation in IgG4-related disease. Ann Rheum Dis. 2015;74(12):2236–43.
doi: 10.1136/annrheumdis-2014-205799 pubmed: 25143523
Allard-Chamard H, Kaneko N, Bertocchi A, Sun N, Boucau J, Kuo HH, Farmer JR, Perugino C, Mahajan VS, Murphy SJH, et al. Extrafollicular IgD(-)CD27(-)CXCR5(-)CD11c(-) DN3 B cells infiltrate inflamed tissues in autoimmune fibrosis and in severe COVID-19. Cell Rep. 2023;42(6):112630.
doi: 10.1016/j.celrep.2023.112630 pubmed: 37300833 pmcid: 10227203
Cai S, Hu Z, Chen Y, Zhong J, Dong L. Potential roles of non-lymphocytic cells in the pathogenesis of IgG4-related disease. Front Immunol. 2022;13:940581.
doi: 10.3389/fimmu.2022.940581 pubmed: 35967331 pmcid: 9366038
Della-Torre E, Lanzillotta M, Doglioni C. Immunology of IgG4-related disease. Clin Exp Immunol. 2015;181(2):191–206.
doi: 10.1111/cei.12641 pubmed: 25865251 pmcid: 4516435
Wu X, Peng Y, Li J, Zhang P, Liu Z, Lu H, Peng L, Zhou J, Fei Y, Zeng X, et al. Single-cell sequencing of Immune Cell Heterogeneity in IgG4-Related disease. Front Immunol. 2022;13:904288.
doi: 10.3389/fimmu.2022.904288 pubmed: 35693817 pmcid: 9184520
Li Y, Wang Z, Han F, Zhang M, Yang T, Chen M, Du J, Wang Y, Zhu L, Hou H et al. Single-cell transcriptome analysis profiles cellular and molecular alterations in submandibular gland and blood in IgG4-related disease. Ann Rheum Dis 2023.
Wallace ZS, Naden RP, Chari S, Choi H, Della-Torre E, Dicaire JF, Hart PA, Inoue D, Kawano M, Khosroshahi A, et al. The 2019 American College of Rheumatology/European League against Rheumatism Classification Criteria for IgG4-Related disease. Arthritis Rheumatol. 2020;72(1):7–19.
doi: 10.1002/art.41120 pubmed: 31793250
Hao Y, Hao S, Andersen-Nissen E, Mauck WM 3rd, Zheng S, Butler A, Lee MJ, Wilk AJ, Darby C, Zager M, et al. Integrated analysis of multimodal single-cell data. Cell. 2021;184(13):3573–3587e3529.
doi: 10.1016/j.cell.2021.04.048 pubmed: 34062119 pmcid: 8238499
Wu T, Hu E, Xu S, Chen M, Guo P, Dai Z, Feng T, Zhou L, Tang W, Zhan L, et al. clusterProfiler 4.0: a universal enrichment tool for interpreting omics data. Innov (Camb). 2021;2(3):100141.
Fujita Y, Jin D, Mimura M, Sato Y, Takai S, Kida T. Activation of mast-cell-derived chymase in the lacrimal glands of patients with IgG4-Related Ophthalmic Disease. Int J Mol Sci 2022, 23(5).
Bretaud S, Guillon E, Karppinen SM, Pihlajaniemi T, Ruggiero F. Collagen XV, a multifaceted multiplexin present across tissues and species. Matrix Biol Plus. 2020;6–7:100023.
doi: 10.1016/j.mbplus.2020.100023 pubmed: 33543021 pmcid: 7852327
Takaya K, Asou T, Kishi K. Identification of Apolipoprotein D as a dermal fibroblast marker of human aging for development of skin rejuvenation therapy. Rejuvenation Res. 2023;26(2):42–50.
doi: 10.1089/rej.2022.0056 pubmed: 36571249
Joseph DB, Henry GH, Malewska A, Reese JC, Mauck RJ, Gahan JC, Hutchinson RC, Malladi VS, Roehrborn CG, Vezina CM, et al. Single-cell analysis of mouse and human prostate reveals novel fibroblasts with specialized distribution and microenvironment interactions. J Pathol. 2021;255(2):141–54.
doi: 10.1002/path.5751 pubmed: 34173975 pmcid: 8429220
Terao C, Ota M, Iwasaki T, Shiokawa M, Kawaguchi S, Kuriyama K, Kawaguchi T, Kodama Y, Yamaguchi I, Uchida K, et al. IgG4-related disease in the Japanese population: a genome-wide association study. Lancet Rheumatol. 2019;1(1):E14–E22.
doi: 10.1016/S2665-9913(19)30006-2 pubmed: 38229354
Khosroshahi A, Bloch DB, Deshpande V, Stone JH. Rituximab therapy leads to rapid decline of serum IgG4 levels and prompt clinical improvement in IgG4-related systemic disease. Arthritis Rheum. 2010;62(6):1755–62.
doi: 10.1002/art.27435 pubmed: 20191576
Detlefsen S, Brasen JH, Zamboni G, Capelli P, Kloppel G. Deposition of complement C3c, immunoglobulin (ig)G4 and IgG at the basement membrane of pancreatic ducts and acini in autoimmune pancreatitis. Histopathology. 2010;57(6):825–35.
doi: 10.1111/j.1365-2559.2010.03717.x pubmed: 21166697
Shiokawa M, Kodama Y, Kuriyama K, Yoshimura K, Tomono T, Morita T, Kakiuchi N, Matsumori T, Mima A, Nishikawa Y, et al. Pathogenicity of IgG in patients with IgG4-related disease. Gut. 2016;65(8):1322–32.
doi: 10.1136/gutjnl-2015-310336 pubmed: 26964842
Zaferani A, Talsma DT, Yazdani S, Celie JW, Aikio M, Heljasvaara R, Navis GJ, Pihlajaniemi T, van den Born J. Basement membrane zone collagens XV and XVIII/proteoglycans mediate leukocyte influx in renal ischemia/reperfusion. PLoS ONE. 2014;9(9):e106732.
doi: 10.1371/journal.pone.0106732 pubmed: 25188209 pmcid: 4154753
Clementz AG, Mutolo MJ, Leir SH, Morris KJ, Kucybala K, Harris H, Harris A. Collagen XV inhibits epithelial to mesenchymal transition in pancreatic adenocarcinoma cells. PLoS ONE. 2013;8(8):e72250.
doi: 10.1371/journal.pone.0072250 pubmed: 23991074 pmcid: 3750028
Li C, Liu Y, Li Y, Tai R, Sun Z, Wu Q, Liu Y, Sun C. Collagen XV Promotes ER Stress-Induced Inflammation through Activating Integrin beta1/FAK Signaling Pathway and M1 Macrophage Polarization in Adipose Tissue. Int J Mol Sci 2021, 22(18).
McConathy WJ, Alaupovic P. Studies on the isolation and partial characterization of apolipoprotein D and lipoprotein D of human plasma. Biochemistry. 1976;15(3):515–20.
doi: 10.1021/bi00648a010 pubmed: 56198
Costello L, Dicolandrea T, Tasseff R, Isfort R, Bascom C, von Zglinicki T, Przyborski S. Tissue engineering strategies to bioengineer the ageing skin phenotype in vitro. Aging Cell. 2022;21(2):e13550.
doi: 10.1111/acel.13550 pubmed: 35037366 pmcid: 8844123
Podolsky MJ, Yang CD, Valenzuela CL, Datta R, Huang SK, Nishimura SL, Dallas SL, Wolters PJ, Le Saux CJ, Atabai K. Age-dependent regulation of cell-mediated collagen turnover. JCI Insight 2020, 5(10).
Kundig TM, Bachmann MF, DiPaolo C, Simard JJ, Battegay M, Lother H, Gessner A, Kuhlcke K, Ohashi PS, Hengartner H, et al. Fibroblasts as efficient antigen-presenting cells in lymphoid organs. Science. 1995;268(5215):1343–7.
doi: 10.1126/science.7761853 pubmed: 7761853
Ohyama H, Nishimura F, Meguro M, Takashiba S, Murayama Y, Matsushita S. Counter-antigen presentation: fibroblasts produce cytokines by signalling through HLA class II molecules without inducing T-cell proliferation. Cytokine. 2002;17(4):175–81.
doi: 10.1006/cyto.2001.0976 pubmed: 11991669
Hutton AJ, Polak ME, Spalluto CM, Wallington JC, Pickard C, Staples KJ, Warner JA, Wilkinson TM. Human lung fibroblasts present bacterial antigens to autologous lung th cells. J Immunol. 2017;198(1):110–8.
doi: 10.4049/jimmunol.1600602 pubmed: 27895174
Asam S, Nayar S, Gardner D, Barone F. Stromal cells in tertiary lymphoid structures: architects of autoimmunity. Immunol Rev. 2021;302(1):184–95.
doi: 10.1111/imr.12987 pubmed: 34060101

Auteurs

Shigeru Tanaka (S)

Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba, 260-8670, Japan. stanaka@chiba-u.jp.

Takuya Yamamoto (T)

Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba, 260-8670, Japan.

Arifumi Iwata (A)

Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba, 260-8670, Japan.

Masahiro Kiuchi (M)

Department of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Kota Kokubo (K)

Department of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Tomohisa Iinuma (T)

Department of Otorhinolaryngology/Head & Neck Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.

Takahiro Sugiyama (T)

Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba, 260-8670, Japan.

Toyoyuki Hanazawa (T)

Department of Otorhinolaryngology/Head & Neck Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.

Kiyoshi Hirahara (K)

Department of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Kei Ikeda (K)

Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba, 260-8670, Japan. k-ikeda847@dokkyomed.ac.jp.
Department of Rheumatology, Dokkyo Medical University, 880 Kitakobayashi, Shimotsuga, Tochigi, Mibu, 321 - 0293, Japan. k-ikeda847@dokkyomed.ac.jp.

Hiroshi Nakajima (H)

Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba, 260-8670, Japan.

Classifications MeSH