Updates on immunity and inflammation in Parkinson disease pathology

Joshi, Neeraj; Singh, Sarika

doi:10.1002/jnr.24185

Cited by 96 publications

(74 citation statements)

References 187 publications

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“…Research on immunity in PD has mostly focused on the activation of microglia and astrocytes, and the imbalance of B lymphocytes and T lymphocytes and their subpopulations [28]. Little research has been carried out to elucidate the role of humoral immunity in PD.…”

Section: Discussionmentioning

confidence: 99%

Imbalance of circulating Tfh/Tfr cells in patients with Parkinson’s disease

Zhao

Jin

Zheng

et al. 2020

Preprint

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Background: Follicular helper T (Tfh) cells and follicular regulatory T (Tfr) cells are essential for B cell differentiation, germinal center formation, and humoral immune responses. Immunity and inflammation have been thought to be involved in Parkinson’s disease (PD). In this study, we aimed to identify whether circulating Tfh and Tfr (cTfh and cTfr) cells contribute to PD.Methods: Thirty-nine PD patients and 26 health controls (HCs) were enrolled. The numbers of cTfh (CD4+CXCR5+PD-1+) cells and cTfr (CD4+CXCR5+CD25hiCD127low) cells were analyzed via flow cytometry. The serum concentrations of interleukin (IL)-4, IL-10, IL-21, and transforming growth factor (TGF)-β were examined by cytometric bead array.Results: The percentage of cTfh cells among CD4+ T cells in PD patients was significantly higher than that in HCs [3.68% (2.64%–5.70%) vs 1.94% (1.32%–2.99%), P<0.001], while the percentage of cTfr cells among CD4+ T cells in PD patients was slight decreased but without significance [1.05% (0.62%–1.54%) vs 1.3% (0.63%–1.90%), P>0.05]. The percentage of CD19+ B cells in peripheral blood mononuclear cells was significantly lower in PD patients than in HCs [5.35% (4.13%–9.38%) vs 8.68% (5.61%–12.93%), P=0.014]. The serum concentrations of IL-4, IL-10, IL-21, and TGF-β in PD patients did not differ significantly from those in HCs (P>0.05). However, significant positive correlations were found for the serum concentration of IL-21 with H-Y stage (r=0.356, P=0.026) and UPDRS-III score (r=0.347, P=0.030).Conclusions: These results indicate that an imbalance of cTfh and cTfr cells may be involved in the chronic progression of PD, and IL-21 may be a biomarker for monitoring the severity of this disease.

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Section: Discussionmentioning

confidence: 99%

Imbalance of circulating Tfh/Tfr cells in patients with Parkinson’s disease

Zhao

Jin

Zheng

et al. 2020

Preprint

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“…The disorders considered in the present review are caused by different etiologic factors and display a variety of symptoms that could hardly be reconducted to a unifying pattern. However, regardless of the origin of these diseases, the involvement of processes which share aspects reasonably attributable to inflammation is detectable in their underlying pathogenic mechanisms (Giovannoni et al 2007;Wilcock and Griffin 2013;King et al 2014;Ochoa-Cortes et al 2016;Hamlett et al 2018;Stark et al 2016;Chitnis and Weiner 2017;Labzin et al 2018;Fehily and Fitzgerald 2017;Mizuma and Yenari 2017;Neal and Richardson 2017;Franklin et al 2017;Prata et al 2017;Santos and Ferreira 2017;Joshi and Singh 2017;Thelin et al 2017a;Majd et al 2017;Zhang et al 2017;Zolezzi and Inestrosa 2017). This consideration has also been the object of a recent valuable review (Skaper et al 2018).…”

Section: Concluding Remarks and Perspectivesmentioning

confidence: 99%

The S100B story: from biomarker to active factor in neural injury

Michetti

D’Ambrosi

Toesca

et al. 2018

Journal of Neurochemistry

268

238

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S100B is a Ca -binding protein mainly concentrated in astrocytes. Its levels in biological fluids (cerebrospinal fluid, peripheral and cord blood, urine, saliva, amniotic fluid) are recognized as a reliable biomarker of active neural distress. Although the wide spectrum of diseases in which the protein is involved (acute brain injury, neurodegenerative diseases, congenital/perinatal disorders, psychiatric disorders) reduces its specificity, its levels remain an important aid in monitoring the trend of the disorder. Mounting evidence now points to S100B as a Damage-Associated Molecular Pattern molecule which, when released at high concentration, through its Receptor for Advanced Glycation Endproducts, triggers tissue reaction to damage in a series of different neural disorders. This review addresses this novel scenario, presenting data indicating that S100B levels and/or distribution in the nervous tissue of patients and/or experimental models of different neural disorders, for which the protein is used as a biomarker, are directly related to the progress of the disease: acute brain injury (ischemic/hemorrhagic stroke, traumatic injury), neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis), congenital/perinatal disorders (Down syndrome, spinocerebellar ataxia-1), psychiatric disorders (schizophrenia, mood disorders), inflammatory bowel disease. In many cases, over-expression/administration of the protein induces worsening of the disease, whereas its deletion/inactivation produces amelioration. This review points out that the pivotal role of the protein resulting from these data, opens the perspective that S100B may be regarded as a therapeutic target for these different diseases, which appear to share some common features reasonably attributable to neuroinflammation, regardless their origin.

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“…In Parkinson's disease (PD), the involvement of inflammation in the disease process is supported by data showing the infiltration of activated microglia and T cells in post-mortem PD brains [81,82] Additionally, there is accumulation of proinflammatory cytokines such as TNF-α, IFN-γ, and IL-6 IL-1β in the brain and cerebrospinal fluid of PD patients [83,84]. The PD culprit protein, α-synuclein, is able to bind to several immune receptors and elicits in vitro and in vivo inflammatory response [85]. Local inflammation has been thoroughly reported for PD patients, mainly derived from activated microglia [82,85].…”

Section: Other Amyloid Diseasesmentioning

confidence: 93%

“…The PD culprit protein, α-synuclein, is able to bind to several immune receptors and elicits in vitro and in vivo inflammatory response [85]. Local inflammation has been thoroughly reported for PD patients, mainly derived from activated microglia [82,85]. Protein aggregation in PD extends well beyond the CNS and also affects peripheral autonomic neuronal circuits, such as the enteric nervous system [86].…”

Section: Other Amyloid Diseasesmentioning

confidence: 99%

The Role of Inflammation in Amyloid Diseases

Foguel¹

2019

Amyloid Diseases

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Amyloid diseases are characterized by the abnormal accumulation of proteinaceous aggregates (amyloid fibrils or plaques) in tissues and organs. This class of diseases is also characterized by the presence of inflammation. Amyloid fibrils arise from the partial denaturing and unfolding of native proteins. The accumulation of amyloid fibrils causes tissue damage and elicits local and nonlocal immune cell infiltration into tissue and proinflammatory cytokine production. Moreover, these conditions fuel a vicious cycle that can increase amyloid production and create an environment of chronic inflammation. A chronically inflamed tissue rapidly deteriorates and loses its function. In this chapter, we will discuss important data gathered over the years describing the role of inflammation in amyloid diseases. We will describe how inflammation begins and how it affects disease progression for major amyloid diseases, such as Alzheimer's disease (AD) and hereditary TTR amyloidosis (hATTR). Lastly, we will discuss the recent advancements in treatments for amyloid diseases and how they address inflammation in affected patients.

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Updates on immunity and inflammation in Parkinson disease pathology

Cited by 96 publications

References 187 publications

Imbalance of circulating Tfh/Tfr cells in patients with Parkinson’s disease

Imbalance of circulating Tfh/Tfr cells in patients with Parkinson’s disease

The S100B story: from biomarker to active factor in neural injury

The Role of Inflammation in Amyloid Diseases

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