ZINC-DEFICIENCY - CHANGES IN CYTOKINE PRODUCTION AND T-CELL SUBPOPULATIONS IN PATIENTS WITH HEAD AND NECK-CANCER AND IN NONCANCER SUBJECTS

Citation
As. Prasad et al., ZINC-DEFICIENCY - CHANGES IN CYTOKINE PRODUCTION AND T-CELL SUBPOPULATIONS IN PATIENTS WITH HEAD AND NECK-CANCER AND IN NONCANCER SUBJECTS, Proceedings of the Association of American Physicians, 109(1), 1997, pp. 68-77
Citations number
35
Categorie Soggetti
Medicine, General & Internal
ISSN journal
1081650X
Volume
109
Issue
1
Year of publication
1997
Pages
68 - 77
Database
ISI
SICI code
1081-650X(1997)109:1<68:Z-CICP>2.0.ZU;2-O
Abstract
Cell-mediated immune dysfunctions and susceptibility to infections hav e been observed in zinc-deficient human subjects. In this study, we in vestigated the production of cytokines and characterized the T-cell su bpopulations in three groups of mildly zinc-deficient subjects. These included head and neck cancer patients, healthy volunteers who were fo und to have a dietary deficiency of zinc, and healthy volunteers in wh om we induced zinc deficiency experimentally by dietary means. We used cellular zinc criteria for the diagnosis of zinc deficiency. We assay ed enzyme-linked immunosorbent assay the production of cytokines from phytohemagglutinin-stimulated peripheral blood mononuclear cells and a ssessed by flow cytometry the differences in T-cell subpopulations. Ou r studies showed that the cytokines produced by TH1 cells were particu larly sensitive to zinc status, inasmuch as the production of interleu kin-2 (IL-2) and interferon-gamma were decreased even though the defic iency of zinc was mild in our subjects. TH2 cytokines (IL-4, IL-5, and IL-6) were not affected by zinc deficiency. Natural killer cell lytic activity also was decreased in zinc-deficient subjects. Recruitment o f naive T cells (CD4+CD45RA+) and CD8+ CD73+ CD11b-, precursors of cyt olytic T cells, were decreased in mildly zinc-deficient subjects. An i mbalance between the functions of TH1 and TH2 cells and changes in T-c ell subpopulations are most probably responsible for cell-mediated imm une dysfunctions in zinc deficiency.