B-1 derived anti-Thy-1 B cells in old aged mice develop lymphoma/leukemia with high expression of CD11b and Hamp2 that different from TCL1 transgenic mice

IF 5.2 2区 医学 Q1 GERIATRICS & GERONTOLOGY Immunity & Ageing Pub Date : 2024-04-03 DOI:10.1186/s12979-024-00415-6
Kyoko Hayakawa, Yan Zhou, Susan A. Shinton
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Abstract

Human old aged unmutated chronic lymphocytic leukemia U-CLL are the TCL1+ZAP70+CD5+ B cells. Since CD5 makes the BCR signaling tolerance, ZAP70 increased in U-CLL not only TCL1+ alone. In mice, TCL1 (TCL1A) is the negative from neonate to old aged, as TC–. VH8-12/Vk21-5 is the anti-thymocyte/Thy-1 autoreactive ATA B cell. When ATA μκTg generation in mice, ATA B cells are the neonate generated CD5+ B cells in B-1, and in the middle age, CD5+ can be down or continuously CD5+, then, old aged CLL/lymphoma generation with increased CD11b in TC–ZAP70–CD5– or TC–ZAP70+CD5+. In this old aged TC–ATA B microarray analysis showed most similar to human CLL and U-CLL, and TC–ZAP70+CD5+ showed certain higher present as U-CLL. Original neonate ATA B cells showed with several genes down or further increase in old aged tumor, and old aged T-bet+CD11c+, CTNNB1hi, HMGBhi, CXCR4hi, DPP4hi and decreased miR181b. These old aged increased genes and down miR181b are similar to human CLL. Also, in old age ATA B cell tumor, high CD38++CD44++, increased Ki67+ AID+, and decreased CD180– miR15Olow are similar to U-CLL. In this old aged ATA B, increased TLR7,9 and Wnt10b. TC+Tg generated with ATAμκTg mice occurred middle age tumor as TC+ZAP70–CD5+ or TC+ZAP70+CD5+, with high NF-kB1, TLR4,6 and Wnt5b,6 without increased CD11b. Since neonatal state to age with TC+Tg continuously, middle age CLL/lymphoma generation is not similar to old aged generated, however, some increased in TC+ZAP70+ are similar to the old age TC– ATA B tumor. Then, TC– ATA B old age tumor showed some difference to human CLL. ATA B cells showed CD11b+CD22++, CD24 down, and hepcidin Hamp2++ with iron down. This mouse V8-12 similar to human V2-5, and V2-5 showed several cancers with macrophages/neutrophils generated hepcidin+ ironlow or some showed hepcidin– iron+ with tumor, and mouse V8-12 with different Vk19-17 generate MZ B cells strongly increased macrophage++ in old aged and generated intestine/colon tumor. Conclusion, neonate generated TC–ATA B1 cells in old aged tumor generation are CD11b+ in the leukemia CLL together with lymphoma cancer with hepcidin-related Hamp2++ in B-1 cell generation to control iron.
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老年小鼠 B-1 衍生的抗 Thy-1 B 细胞发生淋巴瘤/白血病,CD11b 和 Hamp2 高表达,与 TCL1 转基因小鼠不同
人类老年未变异慢性淋巴细胞白血病 U-CLL 是 TCL1+ZAP70+CD5+ B 细胞。由于 CD5 使 BCR 信号转导产生耐受性,因此在 U-CLL 中,ZAP70 不仅仅增加了 TCL1+。在小鼠中,TCL1(TCL1A)与 TC- 一样,从新生儿到老年均为阴性。VH8-12/Vk21-5 是抗胸腺细胞/Thy-1 自反应 ATA B 细胞。当小鼠产生 ATA μκTg 时,ATA B 细胞是新生儿产生的 B-1 中的 CD5+ B 细胞,到了中年,CD5+ 可以下降或持续 CD5+,然后,老年 CLL/淋巴瘤产生的 TC-ZAP70-CD5- 或 TC-ZAP70+CD5+ 中 CD11b 增加。在这些老年 TC-ATA B 细胞中,芯片分析表明它们与人类 CLL 和 U-CLL 最为相似,TC-ZAP70+CD5+ 与 U-CLL 有一定的高度相似性。原来的新生 ATA B 细胞在老年肿瘤中显示出多个基因下降或进一步上升,老年 T-bet+CD11c+、CTNNB1hi、HMGBhi、CXCR4hi、DPP4hi 和 miR181b 下降。这些老年基因的增加和 miR181b 的减少与人类 CLL 相似。此外,在老年 ATA B 细胞肿瘤中,CD38+++CD44+++ 高、Ki67+ AID+ 高、CD180- miR15Olow 低也与 U-CLL 相似。在这种老年 ATA B 细胞肿瘤中,TLR7、9 和 Wnt10b 增加。用 ATAμκTg 小鼠产生的 TC+Tg 中年肿瘤为 TC+ZAP70-CD5+ 或 TC+ZAP70+CD5+,NF-kB1、TLR4,6 和 Wnt5b,6 高,CD11b 不增加。从新生儿期到老年期,TC+Tg不断增加,中年期产生的CLL/淋巴瘤与老年期产生的CLL/淋巴瘤并不相似,但TC+ZAP70+中的某些增加与老年期TC- ATA B肿瘤相似。然后,TC- ATA B 老年肿瘤显示出与人类 CLL 的一些差异。ATA B细胞表现为CD11b+CD22++,CD24下降,血钙素Hamp2++,铁下降。该小鼠V8-12与人类V2-5相似,V2-5的巨噬细胞/中性粒细胞生成的肝磷脂酶+铁低或部分显示肝磷脂酶-铁+,而小鼠V8-12与不同的Vk19-17生成的MZ B细胞在老年期巨噬细胞++强烈增加,并生成肠/结肠肿瘤。结论是,新生儿生成的 TC-ATA B1 细胞在老年肿瘤生成中 CD11b+ 在白血病 CLL 和淋巴瘤癌症中与血磷素相关的 Hamp2++ 在 B-1 细胞生成中控制铁。
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来源期刊
Immunity & Ageing
Immunity & Ageing GERIATRICS & GERONTOLOGY-IMMUNOLOGY
CiteScore
10.20
自引率
3.80%
发文量
55
期刊介绍: Immunity & Ageing is a specialist open access journal that was first published in 2004. The journal focuses on the impact of ageing on immune systems, the influence of aged immune systems on organismal well-being and longevity, age-associated diseases with immune etiology, and potential immune interventions to increase health span. All articles published in Immunity & Ageing are indexed in the following databases: Biological Abstracts, BIOSIS, CAS, Citebase, DOAJ, Embase, Google Scholar, Journal Citation Reports/Science Edition, OAIster, PubMed, PubMed Central, Science Citation Index Expanded, SCImago, Scopus, SOCOLAR, and Zetoc.
期刊最新文献
Age-dependent immune profile in healthy individuals: an original study, systematic review and meta-analysis. Biologically informed machine learning modeling of immune cells to reveal physiological and pathological aging process. Review of evidence linking exposure to environmental stressors and associated alterations in the dynamics of immunosenescence (ISC) with the global increase in multiple sclerosis (MS). Distinct immunomodulation elicited by young versus aged extracellular vesicles in bone marrow-derived macrophages. Inhibiting IL11: a novel approach to turning back the clock.
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