Reduced T helper and B lymphocytes in Parkinson's disease

Stevens, Claire H.; Rowe, Dominic B.; Morel-Kopp, Marie-Christine; Orr, Carolyn; Russell, Tonia; Ranola, Madelaine; Ward, Christopher; Halliday, Glenda M.

doi:10.1016/j.jneuroim.2012.07.015

Cited by 173 publications

(185 citation statements)

References 34 publications

Supporting

Mentioning

168

Contrasting

Unclassified

Order By: Relevance

“…The decrease in total lymphocytes was also reported to be due to lower numbers of T (CD3+) and B (CD19+) cells in PD patients. The alterations in CD3+ cells was explained by the reduction in T helper (Th; CD4+) lymphocytes whereas T cytotoxic (CD8+) cells remained unchanged [30,32,33]. Also, the number of ‘naïve' (CD4+CD45RA+) and memory helper (CD4+CD29+) cells was decreased while the number of activated (CD4+CD25+) T cells was markedly increased [30].…”

Section: Inflammatory and Immune Mechanisms Involved In Pdmentioning

confidence: 99%

See 1 more Smart Citation

Depression and Cognitive Impairment in Parkinson's Disease: A Role for Inflammation and Immunomodulation?

Rocha

Reis

Berghe

et al. 2014

Neuroimmunomodulation

View full text Add to dashboard Cite

The etiology of Parkinson's disease (PD) is complex and not fully understood, most probably because of the multiplicity of factors involved. Inflammatory and abnormal immune responses have been hypothesized to play a crucial role in PD. Not only in the brain, but also peripherally, inflammation is believed to contribute to the onset and progression of the neurodegenerative process seen in PD. Furthermore, increased inflammatory responses have been described both in the brain and peripheral blood of PD subjects. Although PD is considered a motor disorder, nonmotor symptoms are extremely frequent and disabling. Cognitive impairment and mood alterations are such symptoms that deserve increased attention since on the one hand they can appear even before typical motor disturbances are recognized, and on the other hand they are associated with high morbidity and mortality. A growing body of evidence suggests the existence of a link between inflammatory-immune responses and the occurrence of depression and cognitive impairment in PD patients. However, not all data are equally conclusive and are sometimes even conflicting. The aim of this brief review is to give an overview of the possible role that inflammation and immunomodulation may play in PD together with their putative impact on mood and cognitive alterations. What clearly emerges from this work is the fact that studies performed until now lack standardized and comparable methods to analyze both clinical and biological parameters. It is thus difficult to conclusively link mood and cognitive changes to underlying pathological mechanisms. Additional studies in this direction are warranted to convincingly establish or refute any causative relation.

show abstract

Section: Inflammatory and Immune Mechanisms Involved In Pdmentioning

confidence: 99%

“…While NK cells rose in number, their activity was described as comparable in PD and control groups [25,35]. On the other hand, another study did not find any differences in NK cell number between PD patients and control subjects [33]. …”

Section: Inflammatory and Immune Mechanisms Involved In Pdmentioning

confidence: 99%

Depression and Cognitive Impairment in Parkinson's Disease: A Role for Inflammation and Immunomodulation?

Rocha

Reis

Berghe

et al. 2014

Neuroimmunomodulation

View full text Add to dashboard Cite

show abstract

“…A previous study has shown an increase in infiltrating peripheral cells in the SN of PD patients (31), and PBMC composition and function are reportedly altered in PD patients (32)(33)(34)(35)(36). To ensure that our observed differences in p11 levels were not related to PBMC composition changes, we also quantified leukocyte composition.…”

Section: Discussionmentioning

confidence: 99%

Alterations of p11 in brain tissue and peripheral blood leukocytes in Parkinson’s disease

Green

Zhang

Tiklová

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Individuals with Parkinson’s disease (PD) often suffer from comorbid depression. P11 (S100A10), a member of the S100 family of proteins, is expressed widely throughout the body and is involved in major depressive disorder and antidepressant response. Central p11 levels are reduced in postmortem tissue from depressed individuals; however, p11 has not yet been investigated in PD patients with depression or those without depression. We investigated p11 levels in postmortem PD brains and assessed whether peripheral p11 levels correlate with disease severity. Substantia nigra, putamen, and cortical p11 protein levels were assessed in postmortem brain samples from PD patients and matched controls. In a different set of postmortem brains, p11 mRNA expression was measured in dopaminergic cells from the substantia nigra. Both p11 protein and mRNA levels were decreased in PD patients. Peripheral p11 protein levels were investigated in distinct leukocyte populations from PD patients with depression and those without depression. Monocyte, natural killer (NK) cell, and cytotoxic T-cell p11 levels were positively associated with the severity of PD, and NK cell p11 levels were positively associated with depression scores. Given that inflammation plays a role in both PD and depression, it is intriguing that peripheral p11 levels are altered in immune cells in both conditions. Our data provide insight into the pathological alterations occurring centrally and peripherally in PD. Moreover, if replicated in other cohorts, p11 could be an easily accessible biomarker for monitoring the severity of PD, especially in the context of comorbid depression.

show abstract

“…However, there is mounting evidence showing the involvement of the adaptive immune system in PD: the observation of T cells in postmortem PD human brains, 26,97 findings in animal PD models [97][98][99][100][101][102] and data suggesting that the peripheral T cell compartment is altered in PD patients. [48][49][50]96,[103][104][105] We will here concentrate on the last aspect, as we believe it to be crucial to evaluate the strengths and weaknesses of the PD patient immune system if we are to harness it to modulate processes in the brain. When studying the T cell compartment one should consider the changes in absolute cell counts, the distribution between the different stages of T cell function (naive, activated, effector/memory), the type of CD4 cells (TCRαβ vs. TCRγδ, CD4 + vs. CD4 + CD8 lo , CD4:CD8 ratio), and the type of effector T cells (Th1/Th2/Th17/Treg, etc).…”

Section: T Cells Are Impaired In Pdmentioning

confidence: 99%

Vaccination strategies for Parkinson disease

Romero‐Ramos

Chelpin

Sanchez-Guajardo

2014

Human Vaccines & Immunotherapeutics

View full text Add to dashboard Cite

Parkinson disease is the second most common neurodegenerative disease in the world, but there is currently no available cure for it. Current treatments only alleviate some of the symptoms for a few years, but they become ineffective in the long run and do not stop the disease. Therefore it is of outmost importance to develop therapeutic strategies that can prevent, stop, or cure Parkinson disease. A very promising target for these therapies is the peripheral immune system due to its probable involvement in the disease and its potential as a tool to modulate neuroinflammation. But for such strategies to be successful, we need to understand the particular state of the peripheral immune system during Parkinson disease in order to avoid its weaknesses. In this review we examine the available data regarding how dopamine regulates the peripheral immune system and how this regulation is affected in Parkinson disease; the specific cytokine profiles observed during disease progression and the alterations documented to date in patients' peripheral blood mononuclear cells. We also review the different strategies used in Parkinson disease animal models to modulate the adaptive immune response to salvage dopaminergic neurons from cell death. After analyzing the evidence, we hypothesize the need to prime the immune system to restore natural tolerance against α-synuclein in Parkinson disease, including at the same time B and T cells, so that T cells can reprogram microglia activation to a beneficial pattern and B cell/IgG can help neurons cope with the pathological forms of α-synuclein.

show abstract

Reduced T helper and B lymphocytes in Parkinson's disease

Cited by 173 publications

References 34 publications

Depression and Cognitive Impairment in Parkinson's Disease: A Role for Inflammation and Immunomodulation?

Depression and Cognitive Impairment in Parkinson's Disease: A Role for Inflammation and Immunomodulation?

Alterations of p11 in brain tissue and peripheral blood leukocytes in Parkinson’s disease

Vaccination strategies for Parkinson disease

Contact Info

Product

Resources

About