FOLLICULAR LYMPHOMAS CAN BE INDUCED TO PRESENT ALLOANTIGEN EFFICIENTLY - A CONCEPTUAL-MODEL TO IMPROVE THEIR TUMOR IMMUNOGENICITY

FOLLICULAR LYMPHOMAS CAN BE INDUCED TO PRESENT ALLOANTIGEN EFFICIENTLY - A CONCEPTUAL-MODEL TO IMPROVE THEIR TUMOR IMMUNOGENICITY
复制标题

DOI:
10.1073/pnas.92.18.8200
复制
发表时间:
1995-08-29
影响因子:
11.1
通讯作者:
NADLER, LM
NADLER, LM
中科院分区:
综合性期刊1区
文献类型:
--
作者:
SCHULTZE, JL;CARDOSO, AA;NADLER, LM

文献摘要

被引文献

相似文献

在携带肿瘤的宿主中,T细胞总是不能诱导临床显著的抗肿瘤免疫反应。尽管模型系统支持肿瘤肽抗原的存在,但肿瘤细胞抗原呈递的关键分子相互作用仍未得到解决。我们证明了人类滤泡性淋巴瘤细胞在呈递异体抗原时效率非常低,尽管它们强烈表达主要的组织相容性复合体和一些粘附和B7共刺激分子的低至中等表达。通过CD40激活滤泡性淋巴瘤细胞诱导或上调粘附和B7共刺激分子,这是修复这种缺陷所必需的。同种异体反应性T细胞能有效识别未受刺激的滤泡淋巴瘤细胞。因此,肿瘤免疫缺陷的纠正不仅需要主要组织相容性复合体的表达,还需要多种粘附和共刺激分子的充分表达。
In the tumor-bearing host, T cells invariably fail to induce a clinically significant antitumor immune response, Although model systems support the existence of tumor peptide antigens, the molecular interactions critical for antigen presentation by the tumor cell remain unresolved, Here, we demonstrate that human follicular lymphoma cells are highly inefficient at presenting alloantigen despite their strong expression of major histocompatibility complex and low-to-intermediate expression of some adhesion and B7 costimulatory molecules, Activation of follicular lymphoma cells via CD40 induces or up-regulates both adhesion and B7 costimulatory molecules essential to repair this defect, More importantly, once primed, alloreactive T cells efficiently recognize unstimulated follicular lymphoma cells. Thus, correction of defective tumor immunity requires not only expression of major histocompatibility complex but also sufficient expression of multiple adhesion and costimulatory molecules.