Cytokine, Chemokine and Immune Activation Pathway Profiles in Celiac Disease: An Immune System Activity Screening by Expression Macroarrays

Unlike animals, plants do not have specialized immune cells and lack an adaptive immune system. Instead, plant cells rely on their unique innate immune system to defend against pathogens and coordinate beneficial interactions with commensal and symbiotic microbes. One of the major convergent points for plant immune signaling is the nucleus, where transcriptome reprogramming is initiated to orchestrate defense responses. Mechanisms that regulate selective transport of nuclear signaling cargo and chromatin activity at the nuclear boundary play a pivotal role in immune activation. This review summarizes the current knowledge of how nuclear membrane-associated core protein and protein complexes, including the nuclear pore complex, nuclear transport receptors, and the nucleoskeleton participate in plant innate immune activation and pathogen resistance. We also discuss the role of their functional counterparts in regulating innate immunity in animals and highlight potential common mechanisms that contribute to nuclear membrane-centered immune regulation in higher eukaryotes.

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ON THE QUESTION OF THE PATHOGENESIS OF HIV-INFECTION: THE ROLE OF IMMUNE ACTIVATION IN PROGRESSION OF DISEASE

Epidemiology and Infectious Diseases (Russian Journal) ◽

10.17816/eid40663 ◽

2012 ◽

Vol 17 (3) ◽

pp. 47-52

Author(s):

G. R. Khasanova ◽

I. G. Mustafin ◽

V. A. Anokhin

Keyword(s):

Immune System ◽

Gut Microbiota ◽

Hiv Infection ◽

Immune Activation ◽

Opportunistic Pathogens ◽

Rate Of Progression ◽

Progression Of Disease ◽

Modern Knowledge

Hyperactivaion of immme system is considered by most investigators as importantfactor, contributing to progression of HIV-infection and development ofAIDS. In the review modern knowledge about mechanisms and results of activation of immune system during HIV-infection are presented. HIV itself, opportunistic pathogens and components of gut microbiota, first of all, endotoxins ofgram-negative bacteria are considered as probable "activators" of immune system. High levels of endotoxin and markers of immune activation are associated with an even greater rate of progression of HIV-infection.

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The effect of dermal benzophenone-2 administration on immune system activity, hypothalamic-pituitary-thyroid axis activity and hematological parameters in male Wistar rats

Toxicology ◽

10.1016/j.tox.2018.04.002 ◽

2018 ◽

Vol 402-403 ◽

pp. 1-8 ◽

Cited By ~ 4

Author(s):

Żaneta Broniowska ◽

Joanna Ślusarczyk ◽

Beata Starek-Świechowicz ◽

Ewa Trojan ◽

Bartosz Pomierny ◽

...

Keyword(s):

Immune System ◽

Wistar Rats ◽

Hematological Parameters ◽

System Activity ◽

Pituitary Thyroid Axis ◽

Male Wistar Rats ◽

Thyroid Axis

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Arteriosclerosis: The Novel Finding of Biofilms and Innate Immune System Activity within the Plaques

Journal of Medical & Surgical Pathology ◽

10.4172/2472-4971.1000135 ◽

2016 ◽

Vol 01 (04) ◽

Cited By ~ 1

Author(s):

Herbert B Allen ◽

Jennifer Boles ◽

Diego Morales ◽

Shefali Ballal ◽

Suresh G Joshi

Keyword(s):

Immune System ◽

Innate Immune System ◽

Innate Immune ◽

The Novel ◽

System Activity

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Reduction of leucocyte cell surface disulfide bonds during immune activation is dynamic as revealed by a quantitative proteomics workflow (SH-IQ)

Open Biology ◽

10.1098/rsob.180079 ◽

2018 ◽

Vol 8 (9) ◽

pp. 180079

Author(s):

Monika Stegmann ◽

A. Neil Barclay ◽

Clive Metcalfe

Keyword(s):

Immune System ◽

Cell Surface ◽

Immune Activation ◽

Disulfide Bonds ◽

Cell Function ◽

Immune Cell ◽

Surface Proteins ◽

Cell Surface Receptors ◽

Surface Receptors ◽

Pathogen Clearance

Communication through cell surface receptors is crucial for maintaining immune homeostasis, coordinating the immune response and pathogen clearance. This is dependent on the interaction of cell surface receptors with their ligands and requires functionally active conformational states. Thus, immune cell function can be controlled by modulating the structure of either the receptor or the ligand. Reductive cleavage of labile disulfide bonds can mediate such an allosteric change, resulting in modulation of the immune system by a hitherto little studied mechanism. Identifying proteins with labile disulfide bonds and determining the extent of reduction is crucial in elucidating the functional result of reduction. We describe a mass spectrometry-based method—thiol identification and quantitation (SH-IQ)—to identify, quantify and monitor such reduction of labile disulfide bonds in primary cells during immune activation. These results provide the first insight into the extent and dynamics of labile disulfide bond reduction in leucocyte cell surface proteins upon immune activation. We show that this process is thiol oxidoreductase-dependent and mainly affects activatory (e.g. CD132, SLAMF1) and adhesion (CD44, ICAM1) molecules, suggesting a mechanism to prevent over-activation of the immune system and excessive accumulation of leucocytes at sites of inflammation.

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The immune system mediates blood-brain barrier damage; possible implications for pathophysiology of neuropsychiatric illnesses

Acta Neuropsychiatrica ◽

10.1017/s0924270800037315 ◽

1995 ◽

Vol 7 (4) ◽

pp. 114-121 ◽

Cited By ~ 9

Author(s):

Y.D. Van Der Werf ◽

M.J.L. De Jongste ◽

G.J. Ter Horst

Keyword(s):

Myocardial Infarction ◽

Immune System ◽

Blood Brain Barrier ◽

Immune Activation ◽

Inflammatory Cytokine ◽

Brain Barrier ◽

Necrosis Factor Alpha ◽

Blood Brain ◽

Tnf Α ◽

The Brain

SummaryIn this investigation the effects of immune activation on the brain are characterized. In order to study this, we used a model for chronic immune activation, the myocardial infarction, and intravenous injections with the pro-inflammatory cytokine Tumour Necrosis Factor alpha (TNF-α). The incentive for this study is the observation that myocardial infarction is accompanied by behavioural and neuronal abnormalities. The effects of myocardial infarction on the brain and its functioning are widespread. In order to examine the mechanism through which this interaction occurs, a group of rats underwent an experimentally induced myocardial infarction whereafter immunohistochemistry was performed on slices of the brain. This experiment revealed regional serum protein extravasation, pointing to leakage of the blood-brain barrier. This process occurred in certain cortical, subcortical and hindbrain areas in discrete patches. The leakage was co-localized with the expression of the immune activation marker ICAM-1. A second group of rats was therefore injected with TNF-α, a major pro-inflammatory cytokine, to assess the involvement of the immune system in the effects shown. This procedure rendered the same results. It is concluded that myocardial infarction may interfere with the integrity of the blood-brain barrier and possibly with brain functioning through activation of the immune system. The relevance for pathophysiological processes is discussed.

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Psychoneuroimmunology of Post-Traumatic Stress Disorder

10.1093/med/9780190259440.003.0021 ◽

2018 ◽

Author(s):

Rebecca Hannah Bind ◽

Carmine M. Pariante

Keyword(s):

Immune System ◽

Immune Function ◽

Psychiatric Disorders ◽

Post Traumatic Stress Disorder ◽

Immune Activation ◽

Traumatic Stress ◽

Stress Disorder ◽

Post Traumatic Stress ◽

Post Traumatic ◽

Immune Changes

This chapter reviews the evidence linking post-traumatic stress disorder (PTSD) with changes in immune function. The chapter starts with a brief explanation of the components of the immune system, including cytokines, and of the mechanisms linking psychological and psychiatric phenomena with changes in immune function (i.e., psychoneuroimmunology). Specific studies on PTSD are then described, including the potential neurobiological and health consequences of these immune changes and, finally, the effects of PTSD treatment on both symptomology and the immune system. While there is a consistent pattern of findings indicating increased immune activation in this condition, there is a paucity of research on the immunological correlates of PTSD, especially compared with the large number of immunological studies on depression and other psychiatric disorders.

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