Genetic immunization for the melanoma antigen MART-1/Melan-A using recombinant adenovirus-transduced murine dendritic cells.
Genetic immunization for the melanoma antigen MART-1/Melan-A using recombinant adenovirus-transduced murine dendritic cells.
复制标题
使用重组腺病毒转导的鼠树突状细胞对黑色素瘤抗原 MART-1/Melan-A 进行基因免疫。
作者：
A. Ribas;L. Butterfield;W. McBride;S. Jilani;L. Bui;Charles M. Vollmer;R. Lau;V. Dissette;B. Hu;Angela Chen;J. Glaspy;J. Economou
树突状细胞(DC)是一种专职的抗原提呈细胞，能处理和递呈抗原肽，并能产生强大的T细胞免疫。为评价人MART-1/Melan-A(MART-1)黑色素瘤抗原的基因免疫方法，建立了小鼠肿瘤模型。将MART-1基因稳定导入免疫原性较差的小鼠纤维肉瘤细胞系(NFSA)。该转基因肿瘤[NFSA(MART1)]在C3Hf/KAM/SED(H-2k)小鼠体内逐渐生长。对NFSA(MART1)挑战的部分保护可以通过IM实现。注射MART-1表达载体或全身注射表达MART-1的腺病毒载体。然而，用携带MART-1基因的腺病毒载体转导的粒-巨噬细胞集落刺激因子/白介素4分化的小鼠树突状细胞免疫可获得较好的保护作用。静脉注射既可实现部分保护，又可实现完全保护。MART-1工程DC的管理。免疫小鼠的脾细胞含有MHC-1类限制的针对MART-1的CTL。这种基因免疫的临床前模型支持人类黑色素瘤的治疗策略。
Dendritic cells (DCs) are professional antigen-presenting cells that process and present antigenic peptides and are capable of generating potent T-cell immunity. A murine tumor model was developed to evaluate methods of genetic immunization to the human MART-1/Melan-A (MART-1) melanoma antigen. A poorly immunogenic murine fibrosarcoma line (NFSA) was stably transfected with the MART-1 gene. This transfected tumor [NFSA(MART1)] grows progressively in C3Hf/Kam/Sed (H-2k) mice. Partial protection against a challenge with NFSA(MART1) could be achieved with i.m. injections of a MART-1 expression plasmid or with systemic administration of an adenovirus vector expressing MART-1. However, superior protection was achieved when granulocyte macrophage colony-stimulating factor/interleukin-4-differentiated murine DCs transduced with an adenovirus vector expressing MART-1 were used for immunization. Both partial and complete protection could be achieved with i.v. administration of MART-1-engineered DCs. Splenocytes from immunized mice contained MHC class 1-restricted CTLs specific for MART-1. This preclinical model of genetic immunization supports a therapeutic strategy for human melanoma.
人类树突状细胞基因转移方法的比较。
影响因子：
6.4
作者：
Arthur,JF;Butterfield,LH;Roth,MD;Bui,LA;Kiertscher,SM;Lau,R;Dubinett,S;Glaspy,J;McBride,WH;Economou,JS
通讯作者：
Economou,JS