Zinc and its role in immunity and inflammation

被引:567
作者
Bonaventura, Paola [1 ,2 ]
Benedetti, Giulia [1 ,2 ]
Albarede, Francis [3 ]
Miossec, Pierre [1 ,2 ]
机构
[1] Univ Lyon 1, Immunogen & Inflammat Unit, Hosp Civils Lyon, Hop Edouard Herriot,EA 4130, F-69365 Lyon, France
[2] Univ Lyon 1, Dept Clin Immunol & Rheumatol, Hosp Civils Lyon, EA 4130,Hop Edouard Herriot, F-69365 Lyon, France
[3] Ecole Normale Super, Lab Geol Lyon, CNRS UMR 5276, F-69634 Lyon, France
关键词
Zinc; Metallothioneins; Inflammation; Cytokines; Immune diseases; Rheumatoid arthritis; ORAL CHOLERA VACCINE; BREAST-CANCER CELLS; RHEUMATOID-ARTHRITIS; DIETARY ZINC; TRANSCRIPTION FACTOR; INTRACELLULAR ZINC; MATRIX METALLOPROTEINASES; MEDIATED INHIBITION; MAMMALIAN-CELLS; LIV-1; SUBFAMILY;
D O I
10.1016/j.autrev.2014.11.008
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Zinc (Zn) nutritional importance has been known for a long time, but in the last decades its importance in immune modulation has arisen. This review aims at describing the mechanisms involved in the regulation of Zn homeostasis and their effects on the immune response focusing on those which are implicated in the physiopathology of rheumatoid arthritis. Zn functions as a modulator of the immune response through its availability, which is tightly regulated by several transporters and regulators. When this mechanism is disturbed, Zn availability is reduced, altering survival, proliferation and differentiation of the cells of different organs and systems and, in particular, cells of the immune system. Zn deficiency affects cells involved in both innate and adaptive immunity at the survival, proliferation and maturation levels. These cells include monocytes, polymorphonuclear-, natural killer-, T-, and B-cells. T cell functions and the balance between the different T helper cell subsets are particularly susceptible to changes in Zn status. While acute Zn deficiency causes a decrease in innate and adaptive immunity, chronic deficiency increases inflammation. During chronic deficiency, the production of pro-inflammatory cytokines increases, influencing the outcome of a large number of inflammatory diseases, including rheumatoid arthritis. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:277 / 285
页数:9
相关论文
共 125 条
[1]   Rheumatoid arthritis and metal compounds - perspectives on the role of oxygen radical detoxification [J].
Aaseth, J ;
Haugen, M ;
Forre, O .
ANALYST, 1998, 123 (01) :3-6
[2]   Ultraviolet-Visible and Fluorescence Spectroscopy Techniques Are Important Diagnostic Tools during the Progression of Atherosclerosis: Diet Zinc Supplementation Retarded or Delayed Atherosclerosis [J].
Abdelhalim, Mohamed Anwar K. ;
Moussa, Sherif A. Abdelmottaleb ;
Al-Mohy, Yanallah Hussain .
BIOMED RESEARCH INTERNATIONAL, 2013, 2013
[3]  
ABDELMAGEED AB, 1990, VET HUM TOXICOL, V32, P456
[4]   Supplementation with zinc, but not vitamin A, improves seroconversion to vibriocidal antibody in children given an oral cholera vaccine [J].
Albert, MJ ;
Qadri, F ;
Wahed, MA ;
Ahmed, T ;
Rahman, ASMH ;
Ahmed, F ;
Bhuiyan, NA ;
Zaman, K ;
Baqui, AH ;
Clemens, JD ;
Black, RE .
JOURNAL OF INFECTIOUS DISEASES, 2003, 187 (06) :909-913
[5]   Marginal dietary zinc deficiency in vivo induces vascular smooth muscle cell apoptosis in large arteries [J].
Allen-Redpath, Keith ;
Ou, Ou ;
Beattie, John H. ;
Kwun, In-Sook ;
Feldmann, Jorg ;
Nixon, Graeme F. .
CARDIOVASCULAR RESEARCH, 2013, 99 (03) :525-534
[6]   Regulation and function of Zip4, the acrodermatitis enteropathica gene [J].
Andrews, Glen K. .
BIOCHEMICAL SOCIETY TRANSACTIONS, 2008, 36 :1242-1246
[7]   Signal transduction pathways, and nuclear translocation of zinc and metallothionein during differentiation of myoblasts [J].
Apostolova, MD ;
Ivanova, IA ;
Cherian, MG .
BIOCHEMISTRY AND CELL BIOLOGY, 2000, 78 (01) :27-37
[8]  
Aschner M, 2005, J ALZHEIMERS DIS, V8, P139
[9]   The ins and outs of biological zinc sites [J].
Auld, David S. .
BIOMETALS, 2009, 22 (01) :141-148
[10]   Zinc modulates mRNA levels of cytokines [J].
Bao, B ;
Prasad, AS ;
Beck, FWJ ;
Godmere, M .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2003, 285 (05) :E1095-E1102