Erratum: Corrigendum: A cytosolic pathway for MHC class II–restricted antigen processing that is proteasome and TAP dependent

Tewari, Mona K; Sinnathamby, Gomathinayagam; Rajagopal, Deepa; Eisenlohr, Laurence C.

doi:10.1038/ni0405-420

Cited by 2 publications

(5 citation statements)

References 1 publication

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“…A third form of autophagy, microautophagy, in which cytosolic proteins are delivered to the late endosome during multivesicular body formation (91), is also likely to contribute to MHCII processing although a direct connection remains to be made. We and others have shown roles for the proteasome (92–95) and even TAP (94) in endogenous processing of some proteins. Like cross-presentation, these observations blur the line between the MHCI and MHCII systems.…”

Section: Alternative Mhcii Processingmentioning

confidence: 91%

“…Following are additional considerations leading up to our proposal for a different way of thinking about MHCII processing:

A cellular component can contribute to different processing schemes. For example, H-2M can contribute to loading of both proteasome-dependent and -independent epitopes (94).

The same epitope can be produced via multiple pathways.

…”

Section: Additional Considerationsmentioning

confidence: 99%

“…For example, H-2M can contribute to loading of both proteasome-dependent and -independent epitopes (94). …”

Section: Additional Considerationsmentioning

confidence: 99%

“…We were first made aware of this possibility by an epitope within the influenza hemagglutinin that is presentable from exogenous antigen via the recycling pathway and from endogenous sources by a proteasome-dependent pathway (73, 94). Since that time we have expanded the analysis, finding that most of the influenza epitopes we have examined, are presentable from both exogenous and endogenous sources of the parent antigen, just much more efficiently in most cases via endogenous sources (unpublished).…”

Section: Additional Considerationsmentioning

confidence: 99%

See 3 more Smart Citations

Toward a Network Model of MHC Class II-Restricted Antigen Processing

2013

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The standard model of Major Histocompatibility Complex class II (MHCII)-restricted antigen processing depicts a straightforward, linear pathway: internalized antigens are converted into peptides that load in a chaperone dependent manner onto nascent MHCII in the late endosome, the complexes subsequently trafficking to the cell surface for recognition by CD4+ T cells (TCD4+). Several variations on this theme, both moderate and radical, have come to light but these alternatives have remained peripheral, the conventional pathway generally presumed to be the primary driver of TCD4+ responses. Here we continue to press for the conceptual repositioning of these alternatives toward the center while proposing that MHCII processing be thought of less in terms of discrete pathways and more in terms of a network whose major and minor conduits are variable depending upon many factors, including the epitope, the nature of the antigen, the source of the antigen, and the identity of the antigen-presenting cell.

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Section: Alternative Mhcii Processingmentioning

confidence: 91%

“…Following are additional considerations leading up to our proposal for a different way of thinking about MHCII processing:

A cellular component can contribute to different processing schemes. For example, H-2M can contribute to loading of both proteasome-dependent and -independent epitopes (94).

The same epitope can be produced via multiple pathways.

…”

Section: Additional Considerationsmentioning

confidence: 99%

“…For example, H-2M can contribute to loading of both proteasome-dependent and -independent epitopes (94). …”

Section: Additional Considerationsmentioning

confidence: 99%

Section: Additional Considerationsmentioning

confidence: 99%

See 2 more Smart Citations

Toward a Network Model of MHC Class II-Restricted Antigen Processing

2013

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“…MHC II and related molecules are expressed by APCs or by other cells after being stimulated by IFN-γ. MHC II molecules mainly load extracellular antigens in the late endosomal MHC II inclusion compartment (MIIC), and also load a part of endogenous antigens via a variety of intracellular pathways [ 234 , 235 ], which are presented to CD4 + T cells [ 233 , 236 ]. It is important to note that an extra mechanism of loading exogenous antigens onto MHC I molecules occurs through a process called cross-presentation [ 237 ].…”

Section: Autophagy and The Innate Immunity In Viral Infectionsmentioning

confidence: 99%

The role of autophagy in viral infections

Chen

Ding

et al. 2023

J Biomed Sci

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Autophagy is an evolutionarily conserved catabolic cellular process that exerts antiviral functions during a viral invasion. However, co-evolution and co-adaptation between viruses and autophagy have armed viruses with multiple strategies to subvert the autophagic machinery and counteract cellular antiviral responses. Specifically, the host cell quickly initiates the autophagy to degrade virus particles or virus components upon a viral infection, while cooperating with anti-viral interferon response to inhibit the virus replication. Degraded virus-derived antigens can be presented to T lymphocytes to orchestrate the adaptive immune response. Nevertheless, some viruses have evolved the ability to inhibit autophagy in order to evade degradation and immune responses. Others induce autophagy, but then hijack autophagosomes as a replication site, or hijack the secretion autophagy pathway to promote maturation and egress of virus particles, thereby increasing replication and transmission efficiency. Interestingly, different viruses have unique strategies to counteract different types of selective autophagy, such as exploiting autophagy to regulate organelle degradation, metabolic processes, and immune responses. In short, this review focuses on the interaction between autophagy and viruses, explaining how autophagy serves multiple roles in viral infection, with either proviral or antiviral functions.

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Erratum: Corrigendum: A cytosolic pathway for MHC class II–restricted antigen processing that is proteasome and TAP dependent

Abstract: On page 289, the top row of Figure 3a did not include error bars for the primary B cell columns S3 and NA79. The correct Figure 3a, including all error bars, is below.

Cited by 2 publications

References 1 publication

Toward a Network Model of MHC Class II-Restricted Antigen Processing

Toward a Network Model of MHC Class II-Restricted Antigen Processing

The role of autophagy in viral infections

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