Antigen presentation between T cells drives Th17 polarization under conditions of limiting antigen

T cells form immunological synapses with professional antigen-presenting cells (APCs) resulting in T cell activation and the acquisition of peptide antigen-MHC (pMHC) complexes from the plasma membrane of the APC. They thus become APCs themselves. We investigate the functional outcome of T-T cell an...

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Detalles Bibliográficos
Autores: Boccasavia, Viola L., Bovolenta, Elena R., Villanueva, Alberto, Borroto Revuelta, Aldo, Oeste, Clara L., Santen, Hisse M. van, Prieto López, Cristina, Alonso-López, D., Díaz-Muñoz, Manuel D., Batista, Facundo D., Alarcón, Balbino
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2021
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/241754
Acceso en línea:http://hdl.handle.net/10261/241754
Access Level:acceso abierto
Palabra clave:Antigen presentation by T cells
Trogocytosis
Th17
Treg
Limiting antigen
Vaccine dosing
Descripción
Sumario:T cells form immunological synapses with professional antigen-presenting cells (APCs) resulting in T cell activation and the acquisition of peptide antigen-MHC (pMHC) complexes from the plasma membrane of the APC. They thus become APCs themselves. We investigate the functional outcome of T-T cell antigen presentation by CD4 T cells and find that the antigen-presenting T cells (Tpres) predominantly differentiate into regulatory T cells (Treg), whereas T cells that have been stimulated by Tpres cells predominantly differentiate into Th17 pro-inflammatory cells. Using mice deficient in pMHC uptake by T cells, we show that T-T antigen presentation is important for the development of experimental autoimmune encephalitis and Th17 cell differentiation in vivo. By varying the professional APC:T cell ratio, we can modulate Treg versus Th17 differentiation in vitro and in vivo, suggesting that T-T antigen presentation underlies proinflammatory responses in conditions of antigen scarcity.