日期:
2020 年 — 2026 年
2020
2021
2022
2023
2024
2025
2026
影响因子:

B-1 cells contribute to increased total IgM and shape IgG autoreactivity profiles in Lyn-/- mice but are not a major source of lupus-associated pathogenic autoantibodies

B-1细胞有助于Lyn-/-小鼠体内总IgM水平升高并影响IgG自身反应谱,但并非狼疮相关致病性自身抗体的主要来源。

Ottens, Kristina; Satterthwaite, Anne B

B-1a Cells, but Not Marginal Zone B Cells, Are Implicated in the Accumulation of Autoreactive Plasma Cells in Lyn-/- Mice

B-1a细胞(而非边缘区B细胞)与Lyn-/-小鼠体内自身反应性浆细胞的积累有关。

Ottens, Kristina; Schneider, Jalyn; Satterthwaite, Anne B

T-bet-expressing B cells contribute to the autoreactive plasma cell pool in Lyn(-/-) mice

在Lyn(-/-)小鼠中,表达T-bet的B细胞是自身反应性浆细胞库的组成部分。

Ottens, Kristina; Schneider, Jalyn; Satterthwaite, Anne B

TLR7 Signaling in Lupus B Cells: New Insights into Synergizing Factors and Downstream Signals

狼疮B细胞中的TLR7信号传导:协同因子和下游信号的新见解

Satterthwaite, Anne B

Recent Advances in Lupus B Cell Biology: PI3K, IFNγ, and Chromatin

狼疮B细胞生物学最新进展:PI3K、IFNγ和染色质

Bacalao, Maria A; Satterthwaite, Anne B

PIK3IP1 Promotes Extrafollicular Class Switching in T-Dependent Immune Responses

PIK3IP1促进T细胞依赖性免疫反应中的滤泡外类别转换

Ottens, Kristina; Schneider, Jalyn; Kane, Lawrence P; Satterthwaite, Anne B

Foxo3 Promotes Apoptosis of B Cell Receptor-Stimulated Immature B Cells, Thus Limiting the Window for Receptor Editing.

Foxo3 促进 B 细胞受体刺激的未成熟 B 细胞凋亡,从而限制受体编辑的窗口期

Ottens Kristina, Hinman Rochelle M, Barrios Evan, Skaug Brian, Davis Laurie S, Li Quan-Zhen, Castrillon Diego H, Satterthwaite Anne B

Bruton's Tyrosine Kinase, a Component of B Cell Signaling Pathways, Has Multiple Roles in the Pathogenesis of Lupus

布鲁顿酪氨酸激酶是B细胞信号通路的一个组成部分,在狼疮的发病机制中发挥多种作用。

Satterthwaite, Anne B

Pathways leading to an immunological disease: systemic lupus erythematosus

导致免疫性疾病的途径:系统性红斑狼疮

Zharkova, Olga; Celhar, Teja; Cravens, Petra D; Satterthwaite, Anne B; Fairhurst, Anna-Marie; Davis, Laurie S

Heightened cleavage of Axl receptor tyrosine kinase by ADAM metalloproteases may contribute to disease pathogenesis in SLE

ADAM金属蛋白酶对Axl受体酪氨酸激酶的过度切割可能与系统性红斑狼疮(SLE)的发病机制有关。

Orme, Jacob J; Du, Yong; Vanarsa, Kamala; Mayeux, Jessica; Li, Li; Mutwally, Azza; Arriens, Cristina; Min, Soyoun; Hutcheson, Jack; Davis, Laurie S; Chong, Benjamin F; Satterthwaite, Anne B; Wu, Tianfu; Mohan, Chandra