Immunohistochemical Study of Presence of T Cells, B Cells, and Macrophages in Periradicular Lesions of Primary Teeth

2008 ◽  
Vol 32 (4) ◽  
pp. 287-293 ◽  
Author(s):  
Michele Bolan ◽  
Daniele de Almeida Lima ◽  
Cláudia Pinto Figueiredo ◽  
Gabriella Di Giunta ◽  
Maria José de Carvalho Rocha
Keyword(s):  
T Cells ◽  
Immune System ◽  
B Cells ◽  
Primary Teeth ◽  
Microscopic Analysis ◽  
Inflammatory Cells ◽  
Periapical Lesions ◽  
Inflammatory Processes ◽  
Local Inflammatory Reaction

BACKGROUND: The periapical lesion is the result of a local inflammatory reaction caused by bacteria and its products present on the root canal. The interaction between inflammatory cells and bacteria elicit both specific and non-specific immune responses. OBJETIVE: Due to the lack of studies evaluating the role of the immune system in periapical lesions of primary teeth and considering the potentially systemic effects that these infections can cause in children, especially because of the immaturity of their immune system, we sought to evaluate the presence of T cells, B cells and macrophages on periradicular lesions in primary teeth. STUDY DESIGN: 14 periradicular lesions were analyzed. The immunohistochemistry technique was performed using CD45RO, CD20, CD68 monoclonal antibodies aiming to identify T cells, B cells and macrophages, respectively. Cells were quantified by microscopic analysis of histological sections. RESULTS: Mean percentage of positive cells CD45RO was 11.76; CD20 was 5.25; CD68 was 10.92. Our results showed that T and B cells and macrophages comprise the majority of the inflammatory infiltrate. CONCLUSION: We concluded that both humoral and cell mediated immune reactions take place in periradicular lesions of primary teeth. The immune system plays an important role on the periradicular inflammatory processes in primary teeth.

scholarly journals The Role of Forkhead Box 1 (FOXO1) in the Immune System: Dendritic Cells, T Cells, B Cells, and Hematopoietic Stem Cells

2017 ◽  
Vol 37 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Adriana Alicia Cabrera-Ortega ◽  
Daniel Feinberg ◽  
Youde Liang ◽  
Carlos Rossa ◽  
Dana T. Graves
Keyword(s):  
Stem Cells ◽  
T Cells ◽  
Dendritic Cells ◽  
Immune System ◽  
B Cells ◽  
Hematopoietic Stem Cells ◽  
Hematopoietic Stem ◽  
Forkhead Box

Virome and Inflammasomes, a Finely Tuned Balance with Important Consequences for the Host Health

2019 ◽  
Vol 26 (6) ◽  
pp. 1027-1044 ◽  
Author(s):  
Giulia Freer ◽  
Fabrizio Maggi ◽  
Mauro Pistello
Keyword(s):  
Immune System ◽  
Human Beings ◽  
Review Of The Literature ◽  
Adaptive Immune ◽  
Downstream Effects ◽  
Host Health ◽  
Inflammatory Processes ◽  
Human Immune ◽  
Immune Defences

Background:The virome is a network of viruses normally inhabiting humans. It forms a conspicuous portion of the so-called microbiome, once generically referred to as resident flora. Indeed, viruses infecting humans without leading to clinical disease are increasingly recognized as part of the microbiome and have an impact on the development of our immune system. In addition, they activate inflammasomes, multiprotein complexes that assemble in cells and that are responsible for the downstream effects of sensing pathogens.Objective:This review aims at summarizing the evidence on the role of the virome in modulating inflammation and emphasizes evidence for Anelloviruses as useful molecular markers to monitor inflammatory processes and immune system competence.Method:We carried out a review of the literature published in the last 5 years and summarized older literature to take into account ground-breaking discoveries concerning inflammasome assembly and virome.Results:A massive amount of data recently emerging demonstrate that the microbiome closely reflects what we eat, and many other unexpected variables. Composition, location, and amount of the microbiome have an impact on innate and adaptive immune defences. Viruses making up the virome contribute to shaping the immune system. Anelloviruses, the best known of such viruses, are present in most human beings, persistently without causing apparent disease. Depending on their interplay with such viruses, inflammasomes instruct host defences to tolerate or forfeit a specific microorganism.Conclusion:The virome plays an important role in shaping human immune defences and contributes to inflammatory processes by quenching or increasing them.

scholarly journals T Cells Limit Accumulation of Aggregate Pathology Following Intrastriatal Injection of α-Synuclein Fibrils

2021 ◽  
pp. 1-19
Author(s):  
Sonia George ◽  
Trevor Tyson ◽  
Nolwen L. Rey ◽  
Rachael Sheridan ◽  
Wouter Peelaerts ◽  
...  
Keyword(s):  
T Cells ◽  
Immune System ◽  
B Cells ◽  
Substantia Nigra ◽  
Adaptive Immune System ◽  
Proteinase K ◽  
T And B Cells ◽  
Adaptive Immune ◽  
Immunocompromised Mice ◽  
The Impact

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.

scholarly journals Induction of autoreactive B cells allows priming of autoreactive T cells.

1991 ◽  
Vol 173 (6) ◽  
pp. 1433-1439 ◽  
Author(s):  
R H Lin ◽  
M J Mamula ◽  
J A Hardin ◽  
C A Janeway
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Cytochrome C ◽  
Autoantibody Production ◽  
Autoreactive T Cells ◽  
Human Cytochrome ◽  
Self Tolerance ◽  
Human Cytochrome C

A novel mechanism for breaking T cell self tolerance is described. B cells induced to make autoantibody by immunization of mice with the non-self protein human cytochrome c can present the self protein mouse cytochrome c to autoreactive T cells in immunogenic form. This mechanism of breaking T cell self tolerance could account for the role of foreign antigens in breaking not only B cell but also T cell self tolerance, leading to sustained autoantibody production in the absence of the foreign antigen.

Abstract WMP73: Peripheral T Cells From MCAO Mice Contribute to Microglial Polarization

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Dan Ye ◽  
Yun Xu
Keyword(s):  
T Cells ◽  
Th17 Cells ◽  
Inflammatory Cells ◽  
Treg Cells ◽  
Experimental Stroke ◽  
Dual Roles ◽  
Microglial Polarization ◽  
Peripheral T Cells ◽  
Anti Inflammatory

Both resident microglia and infiltrated peripheral T cells have been proved to play important roles in the pathology of stroke. It is well accepted that activated microglia exert dual roles, including pro-inflammatory (M1) and anti-inflammatory (M2) functions. However, the mechanism regulating microglial polarization remains elusive. T cells are recruited into the ischemic area within 24 h after stroke, which also exhibit pro-inflammatory (Th1, Th17) and anti-inflammatory (Th2, Treg) functions. The interaction between microglia and T cells after stroke is barely understood, which may be served as modifiers of pathobiology in stroke. Here we described the role of T cells in the microglial polarization in mouse experimental stroke. We isolated T cells from spleens of MCAO mice at 24 h and 72 h, respectively, and then added to cultured microglia for 24 h. Our results indicated that splenic T cells obtained at 24 h after MCAO selectively promoted microglia polarize to a pro-inflammatory (M1) state, while T cells obtained at 72 h, favored microglia polarize to an anti-inflammatory (M2) state. The results of flow cytometry showed that Th1 and Th17 cells increased at 24 h after MCAO while Th2 and Treg cells increased at 72 h after MCAO. This study implicates that distinct subtypes of T cells contribute differentially to microglial polarization after stroke onset. Therefore, treatments aiming at modulating the ratios of T cells to anti-inflammatory cells have the potential to induce microglial polarize to M2 phenotype and improve the outcome of ischemic stroke.

scholarly journals The Role of Tumor-Infiltrating B Cells in Tumor Immunity

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Fei Fei Guo ◽  
Jiu Wei Cui
Keyword(s):  
T Cells ◽  
B Cells ◽  
Tumor Immunity ◽  
Therapeutic Target ◽  
Tumor Biomarker ◽  
Potential Therapeutic Target ◽  
Tumor Inhibition ◽  
Tumor Tissues ◽  
The Relationship

Earlier studies on elucidating the role of lymphocytes in tumor immunity predominantly focused on T cells. However, the role of B cells in tumor immunity has increasingly received better attention in recent studies. The B cells that infiltrate tumor tissues are called tumor-infiltrating B cells (TIBs). It is found that TIBs play a multifaceted dual role in regulating tumor immunity rather than just tumor inhibition or promotion. In this article, latest research advances focusing on the relationship between TIBs and tumor complexity are reviewed, and light is shed on some novel ideas for exploiting TIBs as a possible tumor biomarker and potential therapeutic target against tumors.

scholarly journals Enhanced circulating levels of CD3 cells-derived extracellular vesicles in different forms of pulmonary hypertension

2019 ◽  
Vol 9 (3) ◽  
pp. 204589401986435 ◽  
Author(s):  
Djuro Kosanovic ◽  
Ujjwal Deo ◽  
Henning Gall ◽  
Balachandar Selvakumar ◽  
Susanne Herold ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Pulmonary Hypertension ◽  
Extracellular Vesicles ◽  
Inflammatory Cells ◽  
Circulating Endothelial Cells ◽  
Profound Knowledge ◽  
Life Threatening ◽  
Circulating Levels

It has been shown previously that increased circulating endothelial cells-derived extracellular vesicles represent an important pathological attribute of pulmonary hypertension. Although it is a well-known fact that inflammatory cells may also release extracellular vesicles, and pulmonary hypertension is a disease associated with abnormal inflammation, there is no profound knowledge with regard to the role of inflammatory cells-derived extracellular vesicles. Therefore, our study demonstrated that circulating levels of extracellular vesicles derived from T-cells are enhanced in various pulmonary hypertension forms and that endothelial cells-derived extracellular vesicles may have distinctive profiles in different clinical subgroups of pulmonary hypertension, which still remains as a poorly treatable and life-threatening disorder.

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