RESUMO
Type II alveolar cells (AT2s) are critical for basic respiratory homeostasis and tissue repair after lung injury. Prior studies indicate that AT2s also express major histocompatibility complex class II (MHCII) molecules, but how MHCII expression by AT2s is regulated and how it contributes to host defense remain unclear. Here we show that AT2s express high levels of MHCII independent of conventional inflammatory stimuli, and that selective loss of MHCII from AT2s in mice results in modest worsening of respiratory virus disease following influenza and Sendai virus infections. We also find that AT2s exhibit MHCII presentation capacity that is substantially limited compared to professional antigen presenting cells. The combination of constitutive MHCII expression and restrained antigen presentation may position AT2s to contribute to lung adaptive immune responses in a measured fashion, without over-amplifying damaging inflammation.
Assuntos
Células Epiteliais Alveolares/imunologia , Apresentação de Antígeno/imunologia , Células Apresentadoras de Antígenos/imunologia , Infecções por Orthomyxoviridae/imunologia , Infecções por Respirovirus/imunologia , Animais , Linhagem Celular , Cães , Antígenos de Histocompatibilidade Classe II/imunologia , Inflamação/imunologia , Vírus da Influenza A Subtipo H1N1/imunologia , Pulmão/citologia , Pulmão/imunologia , Macaca mulatta , Células Madin Darby de Rim Canino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Camundongos Knockout , Infecções por Orthomyxoviridae/patologia , Infecções por Respirovirus/patologia , Vírus Sendai/imunologiaRESUMO
Elevated O-GlcNAcylation is emerging as a general characteristic of most cancers. Although O-GlcNAcylation can regulate many cell biological pathways, recent evidence suggests that it is a key regulator of metabolic pathways including glycolysis in cancer cells. This review summarizes our current understanding of how O-GlcNAcylation regulates glycolytic pathways and contributes to alterations in cancer cell metabolism.