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© The Rockefeller University Press, 0022-1007/1996/12/2439/ $5.00
The Journal of Experimental Medicine, Volume 184, Number 6, December 1, 1996 2439-2444

Brief Definitive Reports

CD8β Increases CD8 Coreceptor Function and Participation in TCR–Ligand Binding

Valery Renard*, Pedro Romero{ddagger}, Eric Vivier*, Bernard Malissen*, and Immanuel F. Luescher{ddagger}

From the * Centre d'Immunologie Institut National de la Santé et de la Recherche Médicale, Centre National de la Recherche Scientifique de Marseille-Luminy, Case 906, 13288 Marseille, Cedex 09, France; and {ddagger} Ludwig Institute for Cancer Research, Lausanne Branch, University of Lausanne, 1066 Epalinges, Switzerland

To study the role of CD8β in T cell function, we derived a CD8{alpha}/β– (CD8–/–) T cell hybridoma of the H-2Kd–restricted N9 cytotoxic T lymphocyte clone specific for a photoreactive derivative of the Plasmodium berghei circumsporozoite peptide PbCS 252-260. This hybridoma was transfected either with CD8{alpha} alone or together with CD8β. All three hybridomas released interleukin 2 upon incubation with L cells expressing Kd–peptide derivative complexes, though CD8{alpha}/β cells did so more efficiently than CD8{alpha}/{alpha} and especially CD8–/– cells. More strikingly, only CD8{alpha}/β cells were able to recognize a weak agonist peptide derivative variant. This recognition was abolished by Fab' fragments of the anti-Kd {alpha}3 monoclonal antibody SF11.1.1 or substitution of Kd D-227 with K, both conditions known to impair CD8 coreceptor function. T cell receptor (TCR) photoaffinity labeling indicated that TCR–ligand binding on CD8{alpha}/β cells was ~5- and 20-fold more avid than on CD8{alpha}/a and CD8–/– cells, respectively. SF1-1.1.1 Fab' or Kd mutation D227K reduced the TCR photoaffinity labeling on CD8{alpha}/β cells to approximately the same low levels observed on CD8–/– cells. These results indicate that CD8{alpha}/β is a more efficient coreceptor than CD8{alpha}/{alpha}, because it more avidly strengthens TCR–ligand binding.

Address correspondence to I.F. Luescher, Ludwig Institute for Cancer Research, Ch. des Boveresses 155, 1066 Epalinges, Switzerland.

This work was supported by grants from the Institut National de la Santé et de la Recherche Médicale/Centre National de la Recherche Scientifique, Ligue Nationale Contre le Cancer and Association pour le Recherche sur le Cancer.


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