Limits...
Macroautophagy in Endogenous Processing of Self- and Pathogen-Derived Antigens for MHC Class II Presentation.

Duraes FV, Niven J, Dubrot J, Hugues S, Gannagé M - Front Immunol (2015)

Bottom Line: Through autophagosomes, endogenous self-antigens as well as antigens derived from intracellular pathogens can be delivered to MHC class II compartment and presented to CD4(+) T cells.The pathway will, therefore, impact both peripheral T cell tolerance and the pathogen specific immune response.This review will describe the contribution of autophagy to intracellular presentation of endogenous self- or pathogen-derived antigens via MHC class II and its consequences on CD4(+) T cell responses.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology and Immunology, School of Medicine, University of Geneva , Geneva , Switzerland.

ABSTRACT
Although autophagy is a process that has been studied for several years its link with antigen presentation and T cell immunity has only recently emerged. Autophagy, which means "self-eating," is important to maintain cell homeostasis and refers to a collection of mechanisms that delivers intracellular material for degradation into lysosomes. Among them, macroautophagy pathway has many implications in different biological processes, including innate and adaptive immunity. In particular, macroautophagy can provide a substantial source of intracellular antigens for loading onto MHC class II molecules using the alternative MHC class II pathway. Through autophagosomes, endogenous self-antigens as well as antigens derived from intracellular pathogens can be delivered to MHC class II compartment and presented to CD4(+) T cells. The pathway will, therefore, impact both peripheral T cell tolerance and the pathogen specific immune response. This review will describe the contribution of autophagy to intracellular presentation of endogenous self- or pathogen-derived antigens via MHC class II and its consequences on CD4(+) T cell responses.

No MeSH data available.


MHC class I and class II processing pathways and autophagy. Classically, MHC class I bound antigens are originated from intracellular proteins through proteasomal proteolysis and are transferred to the outer membrane, where the resulting peptides are presented to CD8+ T cells. On the other hand, MHC class II products originate from extracellular antigens, which are endocytosed and delivered to MHC class II containing compartments (MIIC), where they meet newly generated MHC class II molecules. Alternatively, autophagy can deliver cytosolic antigens for MHC class II presentation, via the fusion of autophagosomes and MIIC, for the presentation of antigens to CD4+ T cells.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4585038&req=5

Figure 2: MHC class I and class II processing pathways and autophagy. Classically, MHC class I bound antigens are originated from intracellular proteins through proteasomal proteolysis and are transferred to the outer membrane, where the resulting peptides are presented to CD8+ T cells. On the other hand, MHC class II products originate from extracellular antigens, which are endocytosed and delivered to MHC class II containing compartments (MIIC), where they meet newly generated MHC class II molecules. Alternatively, autophagy can deliver cytosolic antigens for MHC class II presentation, via the fusion of autophagosomes and MIIC, for the presentation of antigens to CD4+ T cells.

Mentions: Classically, MHC class I bound peptides are generated in the cytosol from various intracellular sources, such as cytosolic or nuclear self-proteins, proteins from intracellular pathogens or endogenous tumor antigens (29). Ubiquitinylation often targets these antigens for proteasomal degradation (30). Proteasomal products are then imported into the lumen of the ER by the transporter associated with antigen processing (TAP) (31), where they are loaded on MHC class I heterodimers. Within the ER, peptide binding is required for the correct folding of MHC class I molecules and its release from the ER. Stable peptide–MHCI complexes are exported to the cell surface via the golgi apparatus for presentation to CD8+ T cells (Figure 2).


Macroautophagy in Endogenous Processing of Self- and Pathogen-Derived Antigens for MHC Class II Presentation.

Duraes FV, Niven J, Dubrot J, Hugues S, Gannagé M - Front Immunol (2015)

MHC class I and class II processing pathways and autophagy. Classically, MHC class I bound antigens are originated from intracellular proteins through proteasomal proteolysis and are transferred to the outer membrane, where the resulting peptides are presented to CD8+ T cells. On the other hand, MHC class II products originate from extracellular antigens, which are endocytosed and delivered to MHC class II containing compartments (MIIC), where they meet newly generated MHC class II molecules. Alternatively, autophagy can deliver cytosolic antigens for MHC class II presentation, via the fusion of autophagosomes and MIIC, for the presentation of antigens to CD4+ T cells.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4585038&req=5

Figure 2: MHC class I and class II processing pathways and autophagy. Classically, MHC class I bound antigens are originated from intracellular proteins through proteasomal proteolysis and are transferred to the outer membrane, where the resulting peptides are presented to CD8+ T cells. On the other hand, MHC class II products originate from extracellular antigens, which are endocytosed and delivered to MHC class II containing compartments (MIIC), where they meet newly generated MHC class II molecules. Alternatively, autophagy can deliver cytosolic antigens for MHC class II presentation, via the fusion of autophagosomes and MIIC, for the presentation of antigens to CD4+ T cells.
Mentions: Classically, MHC class I bound peptides are generated in the cytosol from various intracellular sources, such as cytosolic or nuclear self-proteins, proteins from intracellular pathogens or endogenous tumor antigens (29). Ubiquitinylation often targets these antigens for proteasomal degradation (30). Proteasomal products are then imported into the lumen of the ER by the transporter associated with antigen processing (TAP) (31), where they are loaded on MHC class I heterodimers. Within the ER, peptide binding is required for the correct folding of MHC class I molecules and its release from the ER. Stable peptide–MHCI complexes are exported to the cell surface via the golgi apparatus for presentation to CD8+ T cells (Figure 2).

Bottom Line: Through autophagosomes, endogenous self-antigens as well as antigens derived from intracellular pathogens can be delivered to MHC class II compartment and presented to CD4(+) T cells.The pathway will, therefore, impact both peripheral T cell tolerance and the pathogen specific immune response.This review will describe the contribution of autophagy to intracellular presentation of endogenous self- or pathogen-derived antigens via MHC class II and its consequences on CD4(+) T cell responses.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology and Immunology, School of Medicine, University of Geneva , Geneva , Switzerland.

ABSTRACT
Although autophagy is a process that has been studied for several years its link with antigen presentation and T cell immunity has only recently emerged. Autophagy, which means "self-eating," is important to maintain cell homeostasis and refers to a collection of mechanisms that delivers intracellular material for degradation into lysosomes. Among them, macroautophagy pathway has many implications in different biological processes, including innate and adaptive immunity. In particular, macroautophagy can provide a substantial source of intracellular antigens for loading onto MHC class II molecules using the alternative MHC class II pathway. Through autophagosomes, endogenous self-antigens as well as antigens derived from intracellular pathogens can be delivered to MHC class II compartment and presented to CD4(+) T cells. The pathway will, therefore, impact both peripheral T cell tolerance and the pathogen specific immune response. This review will describe the contribution of autophagy to intracellular presentation of endogenous self- or pathogen-derived antigens via MHC class II and its consequences on CD4(+) T cell responses.

No MeSH data available.