Respiratory Syncytial Virus and T Cells: Interplay between the Virus and the Host Adaptive Immune System

2005 ◽  
Vol 2 (2) ◽  
pp. 141-146 ◽  
Author(s):  
T. J. Braciale
2021 ◽  
pp. 1-19
Author(s):  
Sonia George ◽  
Trevor Tyson ◽  
Nolwen L. Rey ◽  
Rachael Sheridan ◽  
Wouter Peelaerts ◽  
...  

Background: α-Synuclein (α-syn) is the predominant protein in Lewy-body inclusions, which are pathological hallmarks of α- synucleinopathies, such as Parkinson’s disease (PD) and multiple system atrophy (MSA). Other hallmarks include activation of microglia, elevation of pro-inflammatory cytokines, as well as the activation of T and B cells. These immune changes point towards a dysregulation of both the innate and the adaptive immune system. T cells have been shown to recognize epitopes derived from α-syn and altered populations of T cells have been found in PD and MSA patients, providing evidence that these cells can be key to the pathogenesis of the disease. Objective To study the role of the adaptive immune system with respect to α-syn pathology. Methods: We injected human α-syn preformed fibrils (PFFs) into the striatum of immunocompromised mice (NSG) and assessed accumulation of phosphorylated α-syn pathology, proteinase K-resistant α-syn pathology and microgliosis in the striatum, substantia nigra and frontal cortex. We also assessed the impact of adoptive transfer of naïve T and B cells into PFF-injected immunocompromised mice. Results: Compared to wildtype mice, NSG mice had an 8-fold increase in phosphorylated α-syn pathology in the substantia nigra. Reconstituting the T cell population decreased the accumulation of phosphorylated α-syn pathology and resulted in persistent microgliosis in the striatum when compared to non-transplanted mice. Conclusion: Our work provides evidence that T cells play a role in the pathogenesis of experimental α-synucleinopathy.


2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Chang Xia ◽  
Xiaoquan Rao ◽  
Jixin Zhong

Although a critical role of adaptive immune system has been confirmed in driving local and systemic inflammation in type 2 diabetes and promoting insulin resistance, the underlying mechanism is not completely understood. Inflammatory regulation has been focused on innate immunity especially macrophage for a long time, while increasing evidence suggests T cells are crucial for the development of metabolic inflammation and insulin resistance since 2009. There was growing evidence supporting the critical implication of T cells in the pathogenesis of type 2 diabetes. We will discuss the available effect of T cells subsets in adaptive immune system associated with the procession of T2DM, which may unveil several potential strategies that could provide successful therapies in the future.


2020 ◽  
Author(s):  
Sonia George ◽  
Trevor Tyson ◽  
Nolwen L. Rey ◽  
Rachael Sheridan ◽  
Wouter Peelaerts ◽  
...  

AbstractBackground: α-Synuclein (α-syn) is the predominant protein in Lewy-body inclusions, which are pathological hallmarks of α-synucleinopathies, such as Parkinson’s disease (PD) and multiple system atrophy (MSA). Other hallmarks include activation of microglia, elevation of pro-inflammatory cytokines, as well as the activation of T and B cells. These immune changes point towards a dysregulation of both the innate and the adaptive immune system. T cells have been shown to recognize epitopes derived from α-syn and altered populations of T cells have been found in PD and MSA patients, providing evidence that these cells can be key to the pathogenesis of the disease. Objective: To study the role of the adaptive immune system with respect to α-syn pathology. Methods: We injected human α-syn preformed fibrils (PFFs) into the striatum of immunocompromised mice (NSG) and assessed accumulation of phosphorylated α-syn pathology, proteinase K-resistant α-syn pathology and microgliosis in the striatum, substantia nigra and frontal cortex. We also assessed the impact of adoptive transfer of naïve T and B cells into PFF-injected immunocompromised mice. Results: Compared to wildtype mice, NSG mice had an 8-fold increase in phosphorylated α-syn pathology in the substantia nigra. Reconstituting the T cell population decreased the accumulation of phosphorylated α-syn pathology and resulted in persistent microgliosis in the striatum when compared to non-transplanted mice. Conclusion: Our work provides evidence that T cells play a role in the pathogenesis of experimental α-synucleinopathy.


Author(s):  
Bing Liu ◽  
Junyan Han ◽  
Xiaohuan Cheng ◽  
Long Yu ◽  
Li Zhang ◽  
...  

AbstractBackgroundCOVID-19 has been widely spreading. We aim to examine adaptive immune cells in non-severe patients with persistent SARS-CoV-2 shedding.Methods37 non-severe patients with persistent SARS-CoV-2 presence transferred to Zhongnan hospital of Wuhan University were retrospectively recruited to PP (persistently positive) group, which was further allocated to PPP group (n=19) and PPN group (n=18), according to their testing results after 7 days (N=negative). Epidemiological, demographic, clinical and laboratory data were collected and analyzed. Data from age- and sex-matched non-severe patients at disease onset (PA [positive on admission] patients, n=37), and lymphocyte subpopulation measurements from matched 54 healthy subjects were extracted for comparison.ResultsCompared with PA patients, PP patients had much improved laboratory findings, including WBCs, neutrophils, lymphocytes, neutrophil-to-lymphocyte ratio, albumin, AST, CRP, SAA, and IL-6. The absolute numbers of CD3+ T cells, CD4+ T cells, and NK cells were significantly higher in PP group than that in PA group, and were comparable to that in healthy controls. PPP subgroup had markedly reduced B cells and T cells compared to PPN group and healthy subjects. Finally, paired results of these lymphocyte subpopulations from 10 PPN patients demonstrated that the number of T cells and B cells significantly increased when the SARS-CoV-2 tests turned negative.ConclusionPersistent SARS-CoV-2 presence in non-severe COVID-19 patients is associated with reduced numbers of adaptive immune cells. Monitoring lymphocyte subpopulations could be clinically meaningful in identifying fully recovered COVID-19 patients.SummaryDefects in adaptive immune system, including reduced T cells and B cells, were frequently observed in non-severe COVID-19 patients with persistent SARS-CoV-2 shedding. Assessment of immune system could be clinically relevant for discharge management.


Author(s):  
Paul Klenerman

How does the immune system respond to such diverse threats, including viruses never encountered previously by us as a species? The inherent diversity in the immune system can be explained by examining how the adaptive immune system is built, in particular the receptors on B and T lymphocytes. ‘The adaptive immune system: a voyage of (non-)self-discovery’ describes B and T cells, receptors, and the creation of antibodies. Antibody genes are not created as a single unit but are made up from smaller parts, generating many more possible combinations. The antibodies that are created from the genetic template are further honed, becoming highly specific to their target.


2020 ◽  
Vol 401 (4) ◽  
pp. 435-446 ◽  
Author(s):  
Sandra Santos-Sierra

AbstractThe immune system has a limited capacity to recognize and fight cells that become cancerous and in cancer patients, the immune system has to seek the right balance between cancer rejection and host-immunosupression. The tumor milieu builds a protective shell and tumor cells rapidly accumulate mutations that promote antigen variability and immune-escape. Therapeutic vaccination of cancer is a promising strategy the success of which depends on a powerful activation of the cells of the adaptive immune system specific for tumor-cell detection and killing (e.g. CD4+ and CD8+ T-cells). In the last decades, the search for novel adjuvants that enhance dendritic cell (DC) function and their ability to prime T-cells has flourished and some Toll-like receptor (TLR) agonists have long been known to be valid immune adjuvants. The implementation of TLR-synthetic agonists in clinical studies of cancer vaccination is replacing the initial use of microbial-derived products with some encouraging results. The purpose of this review is to summarize the latest discoveries of TLR-synthetic agonists with adjuvant potential in anti-cancer vaccination.


2021 ◽  
Vol 8 (5) ◽  
pp. e1036
Author(s):  
Zhaoqi Yan ◽  
Wei Yang ◽  
Hairong Wei ◽  
Marissa N. Dean ◽  
David G. Standaert ◽  
...  

ObjectiveTo determine the activation status and cytokine profiles of CD4+ T cells, CD8+ T cells, and CD19+ B cells from patients with early-stage Parkinson disease (PD) compared with healthy controls (HCs).MethodsPeripheral blood samples from 41 patients with early-stage PD and 40 HCs were evaluated. Peripheral blood mononuclear cells were analyzed by flow cytometry for surface markers and intracellular cytokine production. Correlations of immunologic changes and clinical parameters were analyzed.ResultsAdaptive immunity plays a role in the pathogenesis of PD, yet the contribution of T cells and B cells, especially cytokine production by these cells, is poorly understood. We demonstrate that naive CD4+ and naive CD8+ T cells are significantly decreased in patients with PD, whereas central memory CD4+ T cells are significantly increased in patients with PD. Furthermore, IL-17–producing CD4+ Th17 cells, IL-4–producing CD4+ Th2 cells, and IFN-γ–producing CD8+ T cells are significantly increased in patients with PD. Regarding B cells, we observed a decrease in naive B cells and an increase in nonswitched memory and double-negative B cells. As well, TNF-α–producing CD19+ B cells were significantly increased in patients with PD. Notably, some of the changes observed in CD4+ T cells and B cells were associated with clinical motor disease severity.ConclusionsThese findings suggest that alterations in the adaptive immune system may promote clinical disease in PD by skewing to a more proinflammatory state in the early-stage PD patient cohort. Our study may shed light on potential immunotherapies targeting dysregulated CD4+ T cells, CD8+ T cells, and CD19+ B cells in patients with PD.


2015 ◽  
Author(s):  
Harlan S Robins

Applying highly sensitive modern immune profiling techniques to the blood or inflamed tissue of auto-immune patients with one of the common T-cell mediated diseases fails to detect large clonal expansions or other signs of a dysregulated immune system. Additionally, these new methods have shown that self-reactive T-cells are found in the periphery (and are not completely negatively selected in the thymus as previously believed). Combining these new data with well-established studies in auto-immunity leads to the conjecture that certain auto-immune diseases are likely to be caused by defects in tissue, not by dysregulation of the adaptive immune system. In particular, one hypothesis is that specific tissues up-regulate HLA class 2 genes, presenting epitopes that are bound by CD4+ helper T cells, which facilitates an immune response against the tissue specific cells.


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