Expression of CR1/2 receptor on alloantigen-stimulated mouse T cells.
Antibodies can mediate injury of organ transplants by several mechanisms, including complement activation and interaction with Fc receptors on cells. We tested the hypothesis that antibodies could also cause up-regulation of complement receptors on cells to increase the responses to complement activation by interaction with split products of C3. In our experimental model, B10.A (H-2(a)) cardiac transplants survive significantly longer in C57BL/6 (H-2(b)) immunoglobulin knockout recipients (IgKO) than in their wild-type counterparts. Passive transfer of specific antibodies to donor MHC class I to IgKO recipients of cardiac allografts at the time coinciding with a vigorous cellular infiltration reconstituted acute rejection. We tested the effects of alloantibodies on CR1/2 expression by alloantigen-stimulated T cells. Both CD4(+)/CR1/2(+) and CD8(+)/CR1/2(+) populations of T cells were expanded in C57BL/6 splenocytes stimulated by B10.A alloantigen in 7-day MLR after coculture with endothelial cells sensitized with IgG1 and IgG2b mAb specific to MHC. Endothelial cells sensitized with antibodies also caused an expansion of CD8(+) T cells expressing CR1/2 in lymph node lymphocytes harvested from a C57BL/6 recipient of a B10.A cardiac allograft. These data suggest that antibodies can augment the cellular rejection process through expanding the population of T cells interacting with complement split products.
Qian
Z
Z
Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Bieler
J G
JG
Baldwin
W M
WM
Wasowska
B A
BA
D000818:Animals; D002460:Cell Line; D004730:Endothelium, Vascular; D005434:Flow Cytometry; D016027:Heart Transplantation / Q000276:immunology*; D007519:Isoantigens / Q000494:pharmacology*; D008198:Lymph Nodes / Q000276:immunology; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D017463:Receptors, Complement 3b / Q000235:genetics*; D017464:Receptors, Complement 3d / Q000235:genetics*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*
D007519:Isoantigens; D017463:Receptors, Complement 3b; D017464:Receptors, Complement 3d