Intersection of autophagy with pathways of antigen presentation

Patterson, Natalie L.; Mintern, Justine D.

doi:10.1007/s13238-012-2097-3

Cited by 26 publications

(20 citation statements)

References 69 publications

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“…Autophagy is a host-defense mechanism against mycobacterial infection (55,56) that enhances peptide presentation by DCs (57). In the current study, we have also found that annexin1 regulates autophagy in DCs and that autophagy can serve as an effective system for the delivery of exogenous antigens in cross-presentation (58,59). Furthermore, it has been shown that following efferocytosis, autophagy promotes apoptotic cell degradation (60).…”

Section: Discussionsupporting

confidence: 54%

Annexin1 regulates DC efferocytosis and cross-presentation during Mycobacterium tuberculosis infection

Tzelepis¹,

Verway²,

Daoud³

et al. 2014

J. Clin. Invest.

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Section: Discussionsupporting

confidence: 54%

Annexin1 regulates DC efferocytosis and cross-presentation during Mycobacterium tuberculosis infection

Tzelepis¹,

Verway²,

Daoud³

et al. 2014

J. Clin. Invest.

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“…Peptides or unfolded proteins can bind to MHCII at the cell surface where they are directly displayed for T cell recognition 27 . Similarly autophagocytosis can deliver cytosolic proteins to endosomal compartments for MHCII antigen presentation 28 . Exosome transfer of MHCII molecules, and their cargoes further diversifies the potential conditions for antigen presentation 29 .…”

Section: General Mechanisms Of Antigen Presentation By Mhcii Moleculesmentioning

confidence: 99%

Revisiting nonclassical HLA II functions in antigen presentation: Peptide editing and its modulation

Álvaro-Benito

Freund

2020

HLA

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The nonclassical major histocompatibility complex of class II molecules (ncMHCII) HLA‐DM (DM) and HLA‐DO (DO) feature essential functions for the selection of the peptides that are displayed by classical MHCII proteins (MHCII) for CD4+ Th cell surveillance. Thus, although the binding groove of classical MHCII dictates the main features of the peptides displayed, ncMHCII function defines the preferential loading of peptides from specific cellular compartments and the extent to which they are presented. DM acts as a chaperone for classical MHCII molecules facilitating peptide exchange and thereby favoring the binding of peptide‐MHCII complexes of high kinetic stability mostly in late endosomal compartments. DO on the other hand binds to DM blocking its peptide‐editing function in B cells and thymic epithelial cells, limiting DM activity in these cellular subsets. DM and DO distinct expression patterns therefore define specific antigen presentation profiles that select unique peptide pools for each set of antigen presenting cell. We have come a long way understanding the mechanistic underpinnings of such distinct editing profiles and start to grasp the implications for ncMHCII biological function. DM acts as filter for the selection of immunodominant, pathogen‐derived epitopes while DO blocks DM activity under certain physiological conditions to promote tolerance to self. Interestingly, recent findings have shown that the unexplored and neglected ncMHCII genetic diversity modulates retroviral infection in mouse, and affects human ncMHCII function. This review aims at highlighting the importance of ncMHCII function for CD4+ Th cell responses while integrating and evaluating what could be the impact of distinct editing profiles because of natural genetic variations.

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“…Moreover, it is essential for the survival and function of B1 cells and plasma cells [ 20 ]. ( 5 ) As is illustrated here, autophagy participates in MHCII antigen presentation, and it could impact MHCI presentation as well [ 21 ]. APCs, antigen-presenting cells; CMA, chaperone-mediated autophagy; LAMP-2A, lysosomal-associated membrane protein type 2A; MAP1LC3/LC3, microtubule associated protein 1 light chain 3; ly-HSPA8 and ly-HSP90, lysosomal luminal HSPA8 and HSP90; MIIC, late endosomal MHC class II compartment; MHCI and II, major histocompatibility complex class I and II; IL-6 and -8, interleukin-6 and -8; PM, plasma membrane; TCR, T-cell receptor; TLR, toll-like receptor.…”

Section: Figurementioning

confidence: 99%

Assessing Autophagy in Mouse Models and Patients with Systemic Autoimmune Diseases

Wang

Schall

et al. 2017

Cells

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Autophagy is a tightly regulated mechanism that allows cells to renew themselves through the lysosomal degradation of proteins, which are misfolded or produced in excess, and of damaged organelles. In the context of immunity, recent research has specially attempted to clarify its roles in infection, inflammation and autoimmunity. Autophagy has emerged as a spotlight in several molecular pathways and trafficking events that participate to innate and adaptive immunity. Deregulation of autophagy has been associated to several autoimmune diseases, in particular to systemic lupus erythematosus. Nowadays, however, experimental data on the implication of autophagy in animal models of autoimmunity or patients remain limited. In our investigations, we use Murphy Roths Large (MRL)/lymphoproliferation (lpr) lupus-prone mice as a mouse model for lupus and secondary Sjögren’s syndrome, and, herein, we describe methods applied routinely to analyze different autophagic pathways in different lymphoid organs and tissues (spleen, lymph nodes, salivary glands). We also depict some techniques used to analyze autophagy in lupus patient’s blood samples. These methods can be adapted to the analysis of autophagy in other mouse models of autoinflammatory diseases. The understanding of autophagy implication in autoimmune diseases could prove to be very useful for developing novel immunomodulatory strategies. Our attention should be focused on the fact that autophagy processes are interconnected and that distinct pathways can be independently hyper-activated or downregulated in distinct organs and tissues of the same individual.

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Intersection of autophagy with pathways of antigen presentation

Cited by 26 publications

References 69 publications

Annexin1 regulates DC efferocytosis and cross-presentation during Mycobacterium tuberculosis infection

Annexin1 regulates DC efferocytosis and cross-presentation during Mycobacterium tuberculosis infection

Revisiting nonclassical HLA II functions in antigen presentation: Peptide editing and its modulation

Assessing Autophagy in Mouse Models and Patients with Systemic Autoimmune Diseases

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