IN-VITRO GENERATION OF IFN-GAMMA-PRODUCING LISTERIA-SPECIFIC T-CELLS IS DEPENDENT ON IFN-GAMMA PRODUCTION BY NON-NK CELLS

Citation
F. Song et al., IN-VITRO GENERATION OF IFN-GAMMA-PRODUCING LISTERIA-SPECIFIC T-CELLS IS DEPENDENT ON IFN-GAMMA PRODUCTION BY NON-NK CELLS, Cellular immunology, 160(2), 1995, pp. 211-216
Citations number
38
Categorie Soggetti
Cell Biology",Immunology
Journal title
ISSN journal
00088749
Volume
160
Issue
2
Year of publication
1995
Pages
211 - 216
Database
ISI
SICI code
0008-8749(1995)160:2<211:IGOILT>2.0.ZU;2-9
Abstract
In vitro B-day cultures of naive spleen cells with viable Listeria mon ocytogenes (VLM), but not heat-killed L. monocytogenes, induced CD4(+) T cells that produced IFN-gamma upon secondary antigen stimulation. T he VLM-induced Listeria-specific T cells produced IFN-gamma but lacked expression of IL-2 and IL-4. To study the role of IFN-gamma in the in duction of the IFN-gamma-producing T cells, we added anti-IFN-gamma mA b to the primary culture and analyzed IFN-gamma production upon second ary antigen stimulation. Addition of anti-IFN-gamma mAb to the culture suppressed generation of IFN-gamma-producing CD4(+) T cells, suggesti ng that IFN-gamma is important in the induction of IFN-gamma-producing CD4(+) T cells. Furthermore, our results showed that depletion of NK cells from spleen cells by anti-asialo GM1 antibody plus complement be fore culture enhanced induction of IFN-gamma-producing CD4(+) T cells. Although NK cells are known to produce IFN-gamma, the results indicat e that NK cell-derived IFN-gamma may not be important in induction of the Listeria-specific IFN-gamma-producing CD4(+) T cells in the cultur e system. In addition, we demonstrated that IFN-gamma expression was h igh in CD4+ T cells from cultures of spleen cells with VLM at the prim ary culture level. These results suggest that IFN-gamma derived from T cells may enhance production of IFN-gamma by CD4(+) T cells, while NK cells rather suppress the induction of IFN-gamma-producing CD4(+) T c ells. (C) 1995 Academic Press, Inc.