Stimulated renal tubular epithelial cells induce anergy in CD4+ T cells.
Renal tubular epithelial cells (TEC) can express MHC class II molecules in vitro and in vivo. Their ability to also secrete cytokines and express adhesion molecules suggests a possible immune accessory role for TEC. We have previously documented that TEC process and present antigen to T cell hybridomas. However, engagement of the T cell receptor alone is sufficient to induce IL-2 secretion by T cell hybridomas. We now report that presentation of antigen by TEC to a CD4+ T cell clone results in functional inactivation of the T cells. Despite antigen-specific anergy, these T cells are viable and proliferate in response to IL-2. Furthermore, allogeneic antigen presenting cells were unable to restore the T cell proliferative response, suggesting that the mechanism(s) was not entirely costimulator-dependent.
Singer
G G
GG
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
Yokoyama
H
H
Bloom
R D
RD
Jevnikar
A M
AM
Nabavi
N
N
Kelley
V R
VR
D000818:Animals; D015704:CD4 Antigens / Q000032:analysis*; D002455:Cell Division / Q000187:drug effects; D002999:Clone Cells; D006825:Hybridomas / Q000166:cytology; D007376:Interleukin-2 / Q000494:pharmacology; D007684:Kidney Tubules / Q000166:cytology / Q000502:physiology*; D051379:Mice; D008815:Mice, Inbred Strains; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000502:physiology*
D015704:CD4 Antigens; D007376:Interleukin-2