TY - JOUR
T1 - Neutrophils and T cells: Bidirectional effects and functional interferences
AU - Thewissen, Marielle
AU - Damoiseaux, Jan
AU - van de Gaar, Jose
AU - Tervaer, Jan Willem Cohen
PY - 2011/9
Y1 - 2011/9
N2 - Polymorphonuclear cells (PMN) are widely recognized as sophisticated killers during microbial infections. In recent years. PMN have been shown to interact and functionally interfere with other cells of the immune system. In this study, we investigated PMN-T cell interactions in an in vitro co-culture system. A relative increase in T cells in the co-culture was associated with the upregulation of CD66b expression on PMN. In addition, PMN were found to dose-dependently impair anti-CD3 induced CD4(+) T cell activation, proliferation and viability. In a transwell co-culture system, proliferation of T cells was, however, enhanced which illustrates that suppression was contact-dependent. The addition of an arginase-inhibitor or blocking antibodies against calprotectin, but not myeloperoxidase (MPO), partially restored T cell proliferation. Furthermore, the presence of PMN in the co-culture dose-dependently increased the fraction of IFN-gamma and IL-17 producing T cells and decreased the percentage of IL-10 producing CD4(+) T cells. Altogether, these data show that there is cross-talk between PMN and T cells which, in non-inflammatory conditions, results in the effects described above. Further studies should investigate PMN-T cell functional interference in inflammatory situations and clarify the importance of this PMN-T cell cross-talk in the regulation of the immune response.
AB - Polymorphonuclear cells (PMN) are widely recognized as sophisticated killers during microbial infections. In recent years. PMN have been shown to interact and functionally interfere with other cells of the immune system. In this study, we investigated PMN-T cell interactions in an in vitro co-culture system. A relative increase in T cells in the co-culture was associated with the upregulation of CD66b expression on PMN. In addition, PMN were found to dose-dependently impair anti-CD3 induced CD4(+) T cell activation, proliferation and viability. In a transwell co-culture system, proliferation of T cells was, however, enhanced which illustrates that suppression was contact-dependent. The addition of an arginase-inhibitor or blocking antibodies against calprotectin, but not myeloperoxidase (MPO), partially restored T cell proliferation. Furthermore, the presence of PMN in the co-culture dose-dependently increased the fraction of IFN-gamma and IL-17 producing T cells and decreased the percentage of IL-10 producing CD4(+) T cells. Altogether, these data show that there is cross-talk between PMN and T cells which, in non-inflammatory conditions, results in the effects described above. Further studies should investigate PMN-T cell functional interference in inflammatory situations and clarify the importance of this PMN-T cell cross-talk in the regulation of the immune response.
KW - PMN
KW - T cells
KW - Calprotectin
KW - Arginase
U2 - 10.1016/j.molimm.2011.07.006
DO - 10.1016/j.molimm.2011.07.006
M3 - Article
C2 - 21813180
SN - 0161-5890
VL - 48
SP - 2094
EP - 2101
JO - Molecular Immunology
JF - Molecular Immunology
IS - 15-16
ER -