Acthar Gel Inhibits the Activation of CD4+ and CD8+ T Cells.

IF 1.9 4区 医学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Dale Wright, Kyle Hayes
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引用次数: 1

Abstract

Several inflammatory diseases are characterized by elevated T cell counts and high pro-inflammatory cytokine levels. Inhibiting T cell activity may reduce tissue damage associated with these diseases. Acthar® Gel has potent anti-inflammatory properties, yet little is known about its effect on T cells. This study compared the effects of Acthar, synthetic adrenocorticotropic hormone 1-24 (ACTH1-24) depot, and prednisolone in a murine model of T cell activation. Assessments of CD4+ helper and CD8+ cytotoxic T cells and plasma concentrations of interferon-γ (IFN-γ), interleukin-2 (IL-2), and tumor necrosis factor-α (TNF-α) were made following anti-CD3-activation. Acthar significantly reduced the number of activated CD4+ and CD8+ T cells at amounts comparable to synthetic ACTH1-24 depot or prednisolone. However, Acthar reduced production of IFN-γ, IL-2, and TNF-α significantly more than the other drugs, suggesting that the in vivo immunomodulatory effects of Acthar on T cells are distinct from synthetic ACTH1-24 depot or prednisolone.

Acthar凝胶抑制CD4+和CD8+ T细胞的活化。
一些炎性疾病的特点是升高的T细胞计数和高促炎细胞因子水平。抑制T细胞活性可能减少与这些疾病相关的组织损伤。Acthar®凝胶具有有效的抗炎特性,但对其对T细胞的作用知之甚少。本研究比较了Acthar、合成促肾上腺皮质激素1-24 (ACTH1-24)库和强的松龙在小鼠T细胞活化模型中的作用。在抗cd3激活后,检测CD4+辅助细胞和CD8+细胞毒性T细胞以及血浆中干扰素-γ (IFN-γ)、白细胞介素-2 (IL-2)和肿瘤坏死因子-α (TNF-α)的浓度。Acthar显著降低活化CD4+和CD8+ T细胞的数量,其数量与合成ACTH1-24库或强的松龙相当。然而,与其他药物相比,Acthar显著降低了IFN-γ、IL-2和TNF-α的产生,这表明Acthar对T细胞的体内免疫调节作用不同于合成ACTH1-24库或强的松龙。
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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
78
审稿时长
2.2 months
期刊介绍: Journal of Interferon & Cytokine Research (JICR) provides the latest groundbreaking research on all aspects of IFNs and cytokines. The Journal delivers current findings on emerging topics in this niche community, including the role of IFNs in the therapy of diseases such as multiple sclerosis, the understanding of the third class of IFNs, and the identification and function of IFN-inducible genes.
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