17
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Reprogramming of the immune system during zinc deficiency.

      1 ,
      Annual review of nutrition
      Annual Reviews

      Read this article at

      ScienceOpenPublisherPubMed
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Thymic atrophy, lymphopenia, and compromised cell- and antibody-mediated responses that cause increased rates of infections of longer duration are the immunological hallmarks of zinc deficiency (ZD) in humans and higher animals. As the deficiency advances, a reprogramming of the immune system occurs, beginning with the activation of the stress axis and chronic production of glucocorticoids that accelerate apoptosis among pre-B and -T cells. This reduces lymphopoiesis and causes atrophy of the thymus. In contrast, myelopoiesis is preserved, thereby providing protection for the first line of immune defense or innate immunity. Changes in gene expression for cytokines, DNA repair enzymes, zinc transporters, signaling molecules, etc., suggest that cells of the immune system are attempting to adapt to the stress of suboptimal zinc. Better understanding of the molecular and cellular changes made in response to inadequate zinc should lead to the development of immunotherapeutic interventions.

          Related collections

          Author and article information

          Journal
          Annu Rev Nutr
          Annual review of nutrition
          Annual Reviews
          0199-9885
          0199-9885
          2004
          : 24
          Affiliations
          [1 ] Department of Biochemistry & Molecular Biology, Department of Food Science & Human Nutrition, Michigan State University, East Lansing, Michigan 48824, USA. fraker@msu.edu
          Article
          10.1146/annurev.nutr.24.012003.132454
          15189122
          01126ff4-a4a8-4b19-809a-52296778fb37
          History

          Comments

          Comment on this article

          Related Documents Log