Conditioning of Langerhans cells induced by a primary CD8 T cell response to self-antigen in vivo.
Using a previously described model of autoimmune skin disease, we addressed the question of how CD8 T cell responsiveness to self-Ag is regulated during chronic inflammation. In this model, CD8 T cells expand and induce tissue pathology directed at an epidermal self-Ag. However, we show here that this primary CD8 T cell response prevented subsequent expansion of a second CD8 T cell population with the same specificity. This lack of T cell accumulation was not due to Ag elimination, nor was it due to competition between the two T cell populations. However, skin-specific dendritic cells that present Ag in this model--Langerhans cells--underwent significant phenotypic changes associated with a compromised ability to stimulate naive T cells. Our study suggests that conditioning of dendritic cells may play a role in maintaining unresponsiveness to self-Ag during chronic inflammation.
Center for Immunology, University of Minnesota, Minneapolis, MN 55455, USA.
Dita
D
Mayerova
Liangchun
L
Wang
Laura S
LS
Bursch
Kristin A
KA
Hogquist
D019264:Adoptive Transfer; D000818:Animals; D001324:Autoantigens; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D002465:Cell Movement; D066298:In Vitro Techniques; D007801:Langerhans Cells / Q000166:cytology / Q000276:immunology*; D008213:Lymphocyte Activation; D051379:Mice; D020297:Mice, Congenic; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010047:Ovalbumin / Q000276:immunology; D010446:Peptide Fragments / Q000276:immunology; D010641:Phenotype; D011828:Radiation Chimera / Q000276:immunology
D001324:Autoantigens; C110366:OVA-8; D010446:Peptide Fragments; D010047:Ovalbumin