Dendritic cell responses to self-assembled monolayers of defined chemistries

被引:22
作者
Shankar, Sucharita P. [1 ,2 ]
Petrie, Timothy A. [3 ]
Garcia, Andres J. [3 ]
Babensee, Julia E. [1 ,2 ]
机构
[1] Georgia Inst Technol, Wallace H Coulter Dept Biomed Engn, Atlanta, GA 30332 USA
[2] Emory Univ, Atlanta, GA 30332 USA
[3] Georgia Inst Technol, George W Woodruff Sch Mech Engn, Atlanta, GA 30332 USA
基金
美国国家科学基金会; 美国国家卫生研究院;
关键词
dendritic cells; self-assembled monolayers; apoptosis; adjuvant; TOLL-LIKE RECEPTORS; II-MEDIATED APOPTOSIS; NECROSIS-FACTOR-ALPHA; IMMUNE-RESPONSE; SURFACE-CHEMISTRY; T-CELL; POLY(LACTIC-CO-GLYCOLIC ACID); PROTEIN ADSORPTION; INNATE IMMUNITY; IN-VITRO;
D O I
10.1002/jbm.a.32487
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Biomaterial contact triggers dendritic cell (DC) maturation, to an extent depending on the biomaterial, ultimately enhancing an immune response toward associated antigens, implying a role for biomaterials as adjuvants. Self-assembled monolayers (SAM) of alkanethiols on titanium/gold-coated surfaces presenting different chemistries were used to study effects of biomaterial surface chemistry on DC maturation. Although DCs treated with OH, COOH, or NH2 SAMs showed modest maturation, those treated with CH3 SAMs were least mature, all based on cytospins, allostimulatory capacity, or maturation marker expression. Surprisingly, DCs treated with CH3 SAMs secreted highest levels of proinflammatory tumor necrosis factor-a (TNF-alpha) or interleukin-6 (IL-6) but were least mature. Secretion of anti-inflammatory mediators by DCs treated with CH3 SAMs was not responsible for mitigating DC maturation under these conditions. Interestingly, elevated levels of apoptotic markers were measured associated with DCs and T cells upon CH3 SAMs contact. Since phagocytosis of apoptotic DCs has strong immunosuppressive effects on DCs, more apoptotic DCs on CH3 SAMs may account for lower DC maturation. Finally, higher expression of cytotoxic T lymphocyte associated antigen receptor-4 (CTLA-4) on T cells may imply a mechanism of T cell inhibition on CH3 SAMs. (C) 2009 Wiley Periodicals, Inc. J Biomed Mater Res 92A: 1487-1499, 2010
引用
收藏
页码:1487 / 1499
页数:13
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