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Asialo GM1+ NK cells have opposite roles in the activation of alloreactive cytotoxic T lymphocyte (CTL) response in vitro and in vivo
- Source :
- Acta pathologica, microbiologica, et immunologica Scandinavica. Section C, Immunology. 95(4)
- Publication Year :
- 1987
-
Abstract
- The immuno-regulatory role of AsialoGM1+ murine NK cells in the induction of allogeneic cytotoxic T cell responses was studied in vivo and in vitro. Depletion of ASGM1+ cells from the (CBAxC57BL/6)F1 cells used for the foot-pad immunization of CBA mice greatly reduced the formation of allospecific CTLs. However, highly purified ASGM1+ cells were not efficient stimulators of alloCTLs in vivo by themselves. When the same genetic combination was used in alloCTL stimulation culture in vitro, ASGM1+ cells were seen to suppress the activation of the CTL response. The opposite roles of ASGM1+ cells in the alloCTL activation in vivo and in vitro were seen when both lymphoid cells (spleen cells or peripheral blood cells) and non-lymphoid cells (epidermal cells) were used as stimulators. The data presented in this paper suggest that during the alloCTL activation, ASGM1+ cells have an important enhancing role in vivo; but in vitro these cells suppress the antigen-presenting cells.
- Subjects :
- Isoantigens
Immunology
Mice, Inbred Strains
G(M1) Ganglioside
In Vitro Techniques
Lymphocyte Activation
Glycosphingolipids
Natural killer cell
03 medical and health sciences
Interleukin 21
Mice
0302 clinical medicine
Antigen
medicine
Cytotoxic T cell
Animals
Antigen-presenting cell
030304 developmental biology
Interleukin 3
0303 health sciences
CD40
General Immunology and Microbiology
biology
General Medicine
Cell biology
Killer Cells, Natural
medicine.anatomical_structure
Host vs Graft Reaction
biology.protein
Interleukin 12
Immunization
030215 immunology
T-Lymphocytes, Cytotoxic
Subjects
Details
- ISSN :
- 01080202
- Volume :
- 95
- Issue :
- 4
- Database :
- OpenAIRE
- Journal :
- Acta pathologica, microbiologica, et immunologica Scandinavica. Section C, Immunology
- Accession number :
- edsair.doi.dedup.....a46b90b57d45b187383c3396020d2f99