Kumar Sanjay, Gautam Pramod Kumar, Tomar Munendra Singh, Acharya Arbind
Centre of Advanced Study, Department of Zoology, Faculty of Science, Banaras Hindu University, Varanasi, U.P., 221 005, India.
Immunol Res. 2016 Feb;64(1):313-23. doi: 10.1007/s12026-015-8752-z.
Hsp70, a highly conserved protein, has gained plenty of attention by virtue of its adjuvant capability to induce peptide-specific cytotoxic T lymphocyte responses. In this study, we have investigated the effect of autologous Hsp70-peptide complex (or simply autologous Hsp70) on the expression of CD28 on T cells and its effector functions through macrophage activation. Further, we investigated the effect of Hsp70 on the expression of CD80 and CD86 on macrophages isolated from normal and tumor-bearing host to provide costimulatory signal for T cell activation and secretion of IL-2 and IFN-γ during interaction. We found that treatment of autologous Hsp70 effectively activated TAMs to induce higher expression of CD28 on T cells through T cells-macrophage interaction. Treatment of autologous Hsp70 induces higher expression of CD80 and CD86 on TAMs, as a result, increases B7/CD28 interaction, which in turns activates T cells and induces higher production of IL-2 and IFN-γ, thereby increasing antigen-specific T cell proliferation. With our novel study, we have provided the strong insights into the role of extracellular Hsp70 on the expression of CD28 costimulatory molecule on T cells, which helps in the activation and generation of antigen-specific T cell effector functions in a tumor-bearing host to curb malignancy.
热休克蛋白70(Hsp70)是一种高度保守的蛋白质,因其具有诱导肽特异性细胞毒性T淋巴细胞反应的佐剂能力而备受关注。在本研究中,我们通过巨噬细胞活化研究了自体Hsp70 - 肽复合物(或简称为自体Hsp70)对T细胞上CD28表达及其效应功能的影响。此外,我们研究了Hsp70对从正常宿主和荷瘤宿主分离的巨噬细胞上CD80和CD86表达的影响,以便在相互作用过程中为T细胞活化以及白细胞介素 - 2(IL - 2)和干扰素 - γ(IFN - γ)的分泌提供共刺激信号。我们发现,自体Hsp70处理通过T细胞 - 巨噬细胞相互作用有效地激活肿瘤相关巨噬细胞(TAM),从而诱导T细胞上CD28的更高表达。自体Hsp70处理可诱导TAM上CD80和CD86的更高表达,结果增加了B7/CD28相互作用,进而激活T细胞并诱导更高水平的IL - 2和IFN - γ产生,从而增加抗原特异性T细胞增殖。通过我们的新研究,我们对细胞外Hsp70在T细胞上CD28共刺激分子表达中的作用有了深入了解,这有助于在荷瘤宿主中激活和产生抗原特异性T细胞效应功能以抑制恶性肿瘤。