CD36 and LC3B initiated autophagy in B cells regulates the humoral immune response

He, Chenfei; Wang, Shan; Zhou, Chikai; He, Minghui; Wang, Jin; Ladds, Marcus J.G.W.; Lianoudaki, Danai; Sedimbi, Saikiran K.; Lane, David P.; Westerberg, Lisa S.; Li, Shuijie; Karlsson, Mikael C. I.

doi:10.1080/15548627.2021.1885183

Cited by 35 publications

(33 citation statements)

References 66 publications

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“…In contrast, in the same mouse model Lovegrove et al showed that CD36-dependent parasite sequestration affected the accumulation of IgM in BALF as a marker for the development of acute lung injury (ALI) [30]. However, CD36 deficiency may also affect the production of IgM [31]. Furthermore, CD36 also plays a significant role in proinflammatory cytokine responses and Th1 development, which is important for controlling parasite burden [32].…”

Section: Plos Pathogensmentioning

confidence: 99%

Skeleton binding protein-1-mediated parasite sequestration inhibits spontaneous resolution of malaria-associated acute respiratory distress syndrome

et al. 2021

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Malaria is a hazardous disease caused by Plasmodium parasites and often results in lethal complications, including malaria-associated acute respiratory distress syndrome (MA-ARDS). Parasite sequestration in the microvasculature is often observed, but its role in malaria pathogenesis and complications is still incompletely understood. We used skeleton binding protein-1 (SBP-1) KO parasites to study the role of sequestration in experimental MA-ARDS. The sequestration-deficiency of these SBP-1 KO parasites was confirmed with bioluminescence imaging and by measuring parasite accumulation in the lungs with RT-qPCR. The SBP-1 KO parasites induced similar lung pathology in the early stage of experimental MA-ARDS compared to wildtype (WT) parasites. Strikingly, the lung pathology resolved subsequently in more than 60% of the SBP-1 KO infected mice, resulting in prolonged survival despite the continuous presence of the parasite. This spontaneous disease resolution was associated with decreased inflammatory cytokine expression measured by RT-qPCR and lower expression of cytotoxic markers in pathogenic CD8+ T cells in the lungs of SBP-1 KO infected mice. These data suggest that SBP-1-mediated parasite sequestration and subsequent high parasite load are not essential for the development of experimental MA-ARDS but inhibit the resolution of the disease.

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Section: Plos Pathogensmentioning

confidence: 99%

Skeleton binding protein-1-mediated parasite sequestration inhibits spontaneous resolution of malaria-associated acute respiratory distress syndrome

et al. 2021

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“…The maintenance of the natural activity of B cells, including the autophagy, contributes to explaining the better immune responses against HIV-1 of LTNP. Confirming this, recent findings highlighted a role for autophagy in B cells in the regulation of humoral immune responses [33]. Overall, despite monocyte/macrophage and B cells representing a restricted percentage of total PMBC, maintenance of high expression of TRIM5α in these particular subsets of cells could be one relevant mechanism for the control of HIV infection observed in LTNP.…”

Section: Discussionmentioning

confidence: 62%

High Levels of TRIM5α Are Associated with Xenophagy in HIV-1-Infected Long-Term Nonprogressors

Ciccosanti

Corazzari

Casetti

et al. 2021

Cells

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Autophagy is a lysosomal-dependent degradative mechanism essential in maintaining cellular homeostasis, but it is also considered an ancient form of innate eukaryotic fighting against invading microorganisms. Mounting evidence has shown that HIV-1 is a critical target of autophagy that plays a role in HIV-1 replication and disease progression. In a special subset of HIV-1-infected patients that spontaneously and durably maintain extremely low viral replication, namely, long-term nonprogressors (LTNP), the resistance to HIV-1-induced pathogenesis is accompanied, in vivo, by a significant increase in the autophagic activity in peripheral blood mononuclear cells. Recently, a new player in the battle of autophagy against HIV-1 has been identified, namely, tripartite motif protein 5α (TRIM5α). In vitro data demonstrated that TRIM5α directly recognizes HIV-1 and targets it for autophagic destruction, thus protecting cells against HIV-1 infection. In this paper, we analyzed the involvement of this factor in the control of HIV-1 infection through autophagy, in vivo, in LTNP. The results obtained showed significantly higher levels of TRIM5α expression in cells from LTNP with respect to HIV-1-infected normal progressor patients. Interestingly, the colocalization of TRIM5α and HIV-1 proteins in autophagic vacuoles in LTNP cells suggested the participation of TRIM5α in the autophagy containment of HIV-1 in LTNP. Altogether, our results point to a protective role of TRIM5α in the successful control of the chronic viral infection in HIV-1-controllers through the autophagy mechanism. In our opinion, these findings could be relevant in fighting against HIV-1 disease, because autophagy inducers might be employed in combination with antiretroviral drugs.

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“…As previously mentioned, CD36 is expressed in adipocytes and hepatocytes, but has also been detected in immune cells, such as macrophages and dendritic cells as well as T and B cells (Urban et al, 2001;Corcoran et al, 2002;Won et al, 2008;Couturier et al, 2019). A study published recently by He et al (2021) demonstrated that all peripheral human blood B cell populations express intracellular CD36 except naïve B cells (He et al, 2021). They found that CD36 colocalizes with LC3B upon the induction of autophagy and splenic B cells increase CD36 expression and autophagosome formation after LPS stimulation in vitro.…”

Section: Role Of Cd36 In B Cells In Obesitymentioning

confidence: 92%

“…They found that CD36 colocalizes with LC3B upon the induction of autophagy and splenic B cells increase CD36 expression and autophagosome formation after LPS stimulation in vitro. Interestingly, B cells from CD36 −/− mice have less autophagosome formation upon LPS stimulation (He et al, 2021) and exhibit defects in mitochondrial mobilization and also oxidative phosphorylation (He et al, 2021), as well as, reduced plasma cell formation, subsequent antibody production and proliferation. Remarkably, the expression of CD36 increases in T lymphocytes of adipose tissue and in the liver of mice fed with a HFD, but it is unclear whether it is preferentially expressed by a specific subset of cells (Couturier et al, 2019).…”

Section: Role Of Cd36 In B Cells In Obesitymentioning

confidence: 99%

Alterations in Lysosome Homeostasis in Lipid-Related Disorders: Impact on Metabolic Tissues and Immune Cells

Cabrera-Reyes

Parra-Ruiz

Yuseff

et al. 2021

Front. Cell Dev. Biol.

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Lipid-related disorders, which primarily affect metabolic tissues, including adipose tissue and the liver are associated with alterations in lysosome homeostasis. Obesity is one of the more prevalent diseases, which results in energy imbalance within metabolic tissues and lysosome dysfunction. Less frequent diseases include Niemann-Pick type C (NPC) and Gaucher diseases, both of which are known as Lysosomal Storage Diseases (LSDs), where lysosomal dysfunction within metabolic tissues remains to be fully characterized. Adipocytes and hepatocytes share common pathways involved in the lysosome-autophagic axis, which are regulated by the function of cathepsins and CD36, an immuno-metabolic receptor and display alterations in lipid diseases, and thereby impacting metabolic functions. In addition to intrinsic defects observed in metabolic tissues, cells of the immune system, such as B cells can infiltrate adipose and liver tissues, during metabolic imbalance favoring inflammation. Moreover, B cells rely on lysosomes to promote the processing and presentation of extracellular antigens and thus could also present lysosome dysfunction, consequently affecting such functions. On the other hand, growing evidence suggests that cells accumulating lipids display defective inter-organelle membrane contact sites (MCSs) established by lysosomes and other compartments, which contribute to metabolic dysfunctions at the cellular level. Overall, in this review we will discuss recent findings addressing common mechanisms that are involved in lysosome dysregulation in adipocytes and hepatocytes during obesity, NPC, and Gaucher diseases. We will discuss whether these mechanisms may modulate the function of B cells and how inter-organelle contacts, emerging as relevant cellular mechanisms in the control of lipid homeostasis, have an impact on these diseases.

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CD36 and LC3B initiated autophagy in B cells regulates the humoral immune response

Cited by 35 publications

References 66 publications

Skeleton binding protein-1-mediated parasite sequestration inhibits spontaneous resolution of malaria-associated acute respiratory distress syndrome

Skeleton binding protein-1-mediated parasite sequestration inhibits spontaneous resolution of malaria-associated acute respiratory distress syndrome

High Levels of TRIM5α Are Associated with Xenophagy in HIV-1-Infected Long-Term Nonprogressors

Alterations in Lysosome Homeostasis in Lipid-Related Disorders: Impact on Metabolic Tissues and Immune Cells

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