Remote control of Th17 responses: The lung-CNS axis during EAE

Vijitha, Nirojah; Engel, Daniel R.

doi:10.1002/jlb.1ce0219-072r

Cited by 4 publications

(1 citation statement)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…IL-6 is a pro-inflammatory cytokine which potentiates inflammation. Moreover, TGF-β and IL-6 are critical for the co-induction of pro-inflammatory Th17 cell differentiation from CD4+ T cells, although even IL-1β seems to be involved [15][16][17]. Emerging evidence indicates that Th17 cells and interleukin 17 (IL-17) are associated with chronic inflammation and pathogenesis of human neurodegenerative diseases.…”

Section: The Dual Role Of Mdscsmentioning

confidence: 99%

The Influence of Myeloid-Derived Suppressor Cell Expansion in Neuroinflammation and Neurodegenerative Diseases

Tamberi,

Belloni,

Pugnaloni

et al. 2024

Cells

View full text Add to dashboard Cite

The neuro-immune axis has a crucial function both during physiological and pathological conditions. Among the immune cells, myeloid-derived suppressor cells (MDSCs) exert a pivotal role in regulating the immune response in many pathological conditions, influencing neuroinflammation and neurodegenerative disease progression. In chronic neuroinflammation, MDSCs could lead to exacerbation of the inflammatory state and eventually participate in the impairment of cognitive functions. To have a complete overview of the role of MDSCs in neurodegenerative diseases, research on PubMed for articles using a combination of terms made with Boolean operators was performed. According to the search strategy, 80 papers were retrieved. Among these, 44 papers met the eligibility criteria. The two subtypes of MDSCs, monocytic and polymorphonuclear MDSCs, behave differently in these diseases. The initial MDSC proliferation is fundamental for attenuating inflammation in Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS), but not in amyotrophic lateral sclerosis (ALS), where MDSC expansion leads to exacerbation of the disease. Moreover, the accumulation of MDSC subtypes in distinct organs changes during the disease. The proliferation of MDSC subtypes occurs at different disease stages and can influence the progression of each neurodegenerative disorder differently.

show abstract

Section: The Dual Role Of Mdscsmentioning

confidence: 99%

The Influence of Myeloid-Derived Suppressor Cell Expansion in Neuroinflammation and Neurodegenerative Diseases

Tamberi,

Belloni,

Pugnaloni

et al. 2024

Cells

View full text Add to dashboard Cite

show abstract

Apelin modulates inflammation and leukocyte recruitment in experimental autoimmune encephalomyelitis

Park,

Song,

Jeong

et al. 2024

Nat Commun

View full text Add to dashboard Cite

Demyelination due to autoreactive T cells and inflammation in the central nervous system are principal features of multiple sclerosis (MS), a chronic and highly disabling human disease affecting brain and spinal cord. Here, we show that treatment with apelin, a secreted peptide ligand for the G protein-coupled receptor APJ/Aplnr, is protective in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Apelin reduces immune cell entry into the brain, delays the onset and reduces the severity of EAE. Apelin affects the trafficking of leukocytes through the lung by modulating the expression of cell adhesion molecules that mediate leukocyte recruitment. In addition, apelin induces the internalization and desensitization of its receptor in endothelial cells (ECs). Accordingly, protection against EAE major outcomes of apelin treatment are phenocopied by loss of APJ/Aplnr function, achieved by EC-specific gene inactivation in mice or knockdown experiments in cultured primary endothelial cells. Our findings highlight the importance of the lung-brain axis in neuroinflammation and indicate that apelin targets the transendothelial migration of immune cells into the lung during acute inflammation.

show abstract

Organic solvents and Multiple Sclerosis: the doubled risk dilemma

Seaton,

Baker,

Hedstrom

et al. 2023

Occupational Medicine

View full text Add to dashboard Cite

Background Compensation for industrial disease in the UK may be obtained in two ways. A State scheme includes a list of accepted associations between occupations and diseases with evidence of a causative association. Epidemiological evidence of a doubled risk in the occupation concerned is usually required. This takes no account of variation of exposures within occupations, excluding many occupations where risk is less than doubled. In such cases, compensation for a perceived industrial illness may be obtained in Civil Courts, where excessive exposures can be considered. Aims To show that in the Civil Courts evidence of excessive exposure may lead to compensation for diseases which are not yet compensable as Industrial Injuries in the UK and to draw attention to the association of multiple sclerosis (MS) with solvent exposure. Methods We report the case of an industrial spray painter, who claimed his MS had been caused by high-level exposure to organic solvents, and our examination of the epidemiological evidence submitted. Results The painter received compensation by an out-of-court settlement, despite the overall epidemiological risk in relation to solvent exposure having been shown to be less than doubled. The evidence hinged on individual risk in relation to high exposure, genetic susceptibility and demonstration of a plausible mechanism. Conclusions High organic solvent exposure may lead to the development of MS. Those giving evidence in Court need to be able to discuss the epidemiological and toxicological issues in relation to exposure in the individual case.

show abstract

Remote control of Th17 responses: The lung-CNS axis during EAE

Abstract: Discussion on remote activation of Th17 cells by lung myeloid cells during EAE.

Cited by 4 publications

References 10 publications

The Influence of Myeloid-Derived Suppressor Cell Expansion in Neuroinflammation and Neurodegenerative Diseases

The Influence of Myeloid-Derived Suppressor Cell Expansion in Neuroinflammation and Neurodegenerative Diseases

Apelin modulates inflammation and leukocyte recruitment in experimental autoimmune encephalomyelitis

Organic solvents and Multiple Sclerosis: the doubled risk dilemma

Contact Info

Product

Resources

About