CD26, adenosine deaminase, and adenosine receptors mediate costimulatory signals in the immunological synapse

R. Pacheco, J. M. Martinez-Navio, M. Lejeune, N. Climent, H. Oliva, J. M. Gatell, T. Gallart, J. Mallol, C. Lluis, R. Franco

Resultado de la investigación: Contribución a una revistaArtículorevisión exhaustiva

170 Citas (Scopus)

Resumen

Adenosine deaminase (ADA), a protein whose deficit leads to severe combined immunodeficiency, binds to the cell surface by means of either CD26, A 1 adenosine receptors, or A2B adenosine receptors. The physiological role of these interactions is not well understood. Our results show that by a 3-fold reduction in the EC50 for the antigen, ADA potentiated T cell proliferation in autologous cocultures with antigen-pulsed immature or mature dendritic cells. Costimulation was not due to the enzymatic activity but to the interaction of ADA-CD26 complexes in T cells with an ADA-anchoring protein in dendritic cells. From colocalization studies, it is deduced that ADA colocalizing with adenosine receptors on dendritic cells interact with CD26 expressed on lymphocytes. This costimulatory signal in the immunological synapse leads to a marked increase (3- to 34-fold) in the production of the T helper 1 and proimmflamatory cytokines IFN-γ, TNF-α, and IL-6.

Idioma originalInglés
Páginas (desde-hasta)9583-9588
Número de páginas6
PublicaciónProceedings of the National Academy of Sciences of the United States of America
Volumen102
N.º27
DOI
EstadoPublicada - 5 jul 2005

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