Effects of coal dust with different concentrations of heavy metals on Cu and Zn content in organs and on cytochrome P-450-dependent monooxygenase system in rat liver and kidneys

Abstract

NK, γδ T and NKT cells bridge innate and adaptive responses because although they are of the T cell lineage, they recognize antigens less specifically than αβ T cells, have rapid effects on pathogens, and secrete cytokines influencing B cells and αβ T cells. NK cell activation is controlled by a balance of signaling by activatory and inhibitory receptors, and is often triggered by a relative deficit of self MHC class I. NK cells kill virus-infected and tumor cells by antibody dependent cell-mediated cytotoxicity (ADCC) or perforin/granzyme-mediated cytotoxicity. γδ T cells reside in mucosal and cutaneous epithelia. γδ TCRs bind to non-peptide pathogen and stress antigens that are recognized directly or when presented on CD1c or MHC class Ib. Activated γδ T cells generate CTLs that kill infected target cells by perforin/granzyme-mediated cytotoxicity, as well as Th effectors that secrete cytokines. NKT cells bear a semi-invariant TCRαβ that recognizes glycolipid and lipid ligands presented on CD1d by APCs. Activated NKT cells rapidly secrete chemokines and cytokines that enhance antipathogen and antitumor immune responses while suppressing autoreactivity. NKT cells promote Th1, Th2 and Th17 differentiation and NK cell functions. It is unclear whether activated NKT cells kill target cells by perforin/granzyme-mediated cytotoxicity in vivo.