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
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