Lysosomes and lysosome‐related organelles in immune responses

Watts, Colin

doi:10.1002/2211-5463.13388

Cited by 39 publications

(25 citation statements)

References 153 publications

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“…Thomas Reinheckel and Martina Tholen reviewed how the release of cathepsin proteases from lysosomes may not be a death sentence for the cell, and that cathepsins have other cellular functions compatible with cell survival [ 4 ]. Finally, Colin Watts reviewed the key role of lysosomes and lysosome‐related organelles in innate and adaptive immunity [ 5 ].…”

Section: New Developments In 2022mentioning

confidence: 99%

Innovation and renovation: FEBS Open Bio in 2023

Wright

Rosa

2023

FEBS Open Bio

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Section: New Developments In 2022mentioning

confidence: 99%

Innovation and renovation: FEBS Open Bio in 2023

Wright

Rosa

2023

FEBS Open Bio

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“…Granulocytes and monocytic cells degrade endocytosed or phagocytosed pathogens or tumor antigens. They also present processed antigens on MHCs for further process by T cells (Watts, 2022).…”

Section: Lysosomesmentioning

confidence: 99%

The lysosome as a novel therapeutic target of EGFR-mediated tumor inflammation

et al. 2022

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EGFR-mediated tumors have been targeted to overcome several different malignant cancers. EGFR overexpression and mutations are directly related to the malignancy, which makes the therapy more complicated. One reason for the malignancy is the induction of AP1 followed by inflammation via IL-6 secretion. Current therapeutic strategies to overcome EGFR-mediated tumors are tyrosine kinase inhibitors (TKIs), anti-EGFR monoclonal antibodies, and the combination of these two agents with classic chemotherapy or immune checkpoint inhibitors (ICIs). Although the strategies are straightforward and have shown promising efficacy in several studies, there are still hurdles to overcoming the adverse effects and limited efficacy. This study reviews the current therapeutic strategies to target EGFR family members, how they work, and their effects and limitations. We also suggest developing novel strategies to target EGFR-mediated tumors in a novel approach. A lysosome is the main custodial staff to discard unwanted amounts of EGFR and other receptor tyrosine kinase molecules. Targeting this organelle may be a new approach to overcoming EGFR-mediated cancers.

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“…In contrast, improving lysosomal function ameliorates steatosis and improves glucose homeostasis in livers of obese mice 21,24 . The lysosome also serves as a central hub for innate and adaptive immunity 25,26 . For example, in the context of tissue injury, leukocytic lysosomes play key roles in controlling pathogen elimination, antigen presentation, inflammasome activation, and inflammatory lipid metabolism 25–29 .…”

Section: Introductionmentioning

confidence: 99%

Gamma-interferon-inducible lysosomal thiol reductase maintains cardiac immuno-metabolic homeostasis in heart failure

Wang

Qian

et al. 2022

Preprint

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Heart failure (HF) remains the leading cause of death globally. The progression of HF is characterized by cardiac mitochondrial dysfunction and aberrant inflammatory responses. Although the lysosome has been recognized as the central player for maintaining immuno-metabolic homeostasis in diverse organs in health and disease, the mechanistic insights into the regulation of lysosome-dependent immuno-metabolism in the heart are lacking. Lysosomal reductase Gamma Interferon-Inducible Thiol Reductase (GILT) is the only identified lysosomal reductase that controls more than 11 lysosomal enzymes, and a single nucleotide polymorphism in the coding sequence of GILT has been implicated in promoting cardiovascular risk. Here, we show that GILT expression and activity are reduced in hearts from human patients and mice with HF, respectively. Moreover, cardiomyocyte-specific deletion of GILT (GILT-cKO) results in left ventricular remodeling and dysfunction in the setting of pressure overload. At the cellular level, cardiac GILT deficiency leads to impaired mitochondrial respiration, elevated mitochondrial oxidative stress, and increased NLR Family Pyrin Domain Containing 3(NLRP3)-dependent inflammation in the heart. Mechanistically, inhibition of NLRP3 in primary cardiomyocytes ameliorated the mitochondrial dysfunction in the GILT deficient cells, implicating a causative role of the lysosome-inflammasome axis on regulating cardiac mitochondrial function. Together, these findings elucidate a functional link between cardiac lysosomes, inflammatory responses and mitochondrial respiration. Knowledge gained from this study might speed the development of therapeutic agents to treat patients with HF.

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Lysosomes and lysosome‐related organelles in immune responses

Cited by 39 publications

References 153 publications

Innovation and renovation: FEBS Open Bio in 2023

Innovation and renovation: FEBS Open Bio in 2023

The lysosome as a novel therapeutic target of EGFR-mediated tumor inflammation

Gamma-interferon-inducible lysosomal thiol reductase maintains cardiac immuno-metabolic homeostasis in heart failure

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