Characteris Tics and Causes of Immune Dysfunction Related to Uremia and Dialysis

2008 ◽  
Vol 28 (3_suppl) ◽  
pp. 183-187 ◽  
Author(s):  
Aline Borsato Hauser ◽  
Andréa E. M. Stinghen ◽  
Sawako Kato ◽  
Sérgio Bucharles ◽  
Carlos Aita ◽  
...  

From the immunologic viewpoint, chronic kidney disease (CKD) is characterized by disorders of both the innate and adaptive systems, generating a complex and still not fully understood immune dysfunction. Markers of a chronically activated immune system are closely linked to several complications of CKD and represent powerful predictors for mortality in the CKD population. On the other hand, CKD patients respond poorly to vaccination and to challenges such as bacterial infection. Interestingly, the main causes of death in patients with CKD are cardiovascular and infectious diseases, both being pathologic processes closely linked to immune function. Therefore, accelerated tissue degeneration (as a consequence of chronic inflammation) and increased rate of sepsis (because of a poorly orchestrated immune response) represent the most important targets for interventions aiming to reduce mortality in CKD patients. Understanding the mechanisms behind the immune dysfunction that is peculiar to CKD generates a perspective to improve outcomes in this group of patients.

Author(s):  
Behdad Afzali ◽  
Claudia Kemper

Immunological health relies on a balance between immune responsiveness to foreign pathogens and tolerance to self-components, commensals, food-derived components, and semi-allogeneic fetal antigens. Disruptions of this balance are hallmarks of immunodeficiency diseases, autoimmune diseases, and pregnancy failure. Patients with chronic kidney disease are immunologically unique in demonstrating features of both chronic inflammation and acquired immunodeficiency—predisposing these individuals to the two commonest causes of death, namely cardiovascular disease and sepsis. Defects and abnormalities in almost all components of the immune system can be observed, although it is difficult to say whether the observations denote mechanism or effect. This chapter reviews, briefly, measurable immune system abnormalities in chronic kidney disease and some of the potential underlying mechanisms.


Author(s):  
Sara Fernandes ◽  
◽  
Ana Ferreira ◽  
◽  

Chronic kidney disease is characterized by immune dysfunction that increases predisposition to infections, virus-associated cancers and impaired response to vaccination. The altered immune response is caused by impairment of both innate and adaptive immune systems, as well as other factors that are hallmarks of renal disease, such as uremia, malnutrition, chronic inflammation, mineral bone disease and anemia. The aim of this article is to review the causes and mechanisms that lead to immune dysfunction in patients with chronic kidney disease.


2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Colin R. Young ◽  
Fred E. Yeo

Chronic kidney disease (CKD) and end-stage renal disease (ESRD) represent a spectrum of impaired immunity with effects on cellular immunity, soluble immune factors, and inflammation. As a result, infections due to impaired immune system responses are responsible for significant morbidity in patients with kidney disease. Because of immune dysfunction in CKD, these patients have reduced probability to clear infections and are susceptible to pathogenic effects of common organisms. We present a case of a patient with CKD coinfected withSchistosoma mansoniandBlastocystisspp. This appears to be the first reported association ofSchistosoma mansoniandBlastocystisspp. in a patient with CKD.


The Analyst ◽  
2021 ◽  
Author(s):  
Yong Zhang ◽  
Shanshan Zheng ◽  
Yonghong Mao ◽  
Wei Cao ◽  
Lijun Zhao ◽  
...  

Immunoglobulin G (IgG) molecules modulate an immune response. However, site-specific N-glycosylation signatures of plasma IgG in patients with chronic kidney disease (CKD) remain unclear. This study aimed to propose a...


2020 ◽  
Vol 23 (1) ◽  
pp. 106-115
Author(s):  
M.M. Gadzhikulieva ◽  
◽  
G.V. Volgina ◽  
N.D. Yushchuk ◽  
I.P. Balmasova ◽  
...  

2020 ◽  
Vol 21 (12) ◽  
pp. 4448 ◽  
Author(s):  
Osnat Almogi-Hazan ◽  
Reuven Or

The Cannabis plant contains numerous components, including cannabinoids and other active molecules. The phyto-cannabinoid activity is mediated by the endocannabinoid system. Cannabinoids affect the nervous system and play significant roles in the regulation of the immune system. While Cannabis is not yet registered as a drug, the potential of cannabinoid-based medicines for the treatment of various conditions has led many countries to authorize their clinical use. However, the data from basic and medical research dedicated to medical Cannabis is currently limited. A variety of pathological conditions involve dysregulation of the immune system. For example, in cancer, immune surveillance and cancer immuno-editing result in immune tolerance. On the other hand, in autoimmune diseases increased immune activity causes tissue damage. Immuno-modulating therapies can regulate the immune system and therefore the immune-regulatory properties of cannabinoids, suggest their use in the therapy of immune related disorders. In this contemporary review, we discuss the roles of the endocannabinoid system in immunity and explore the emerging data about the effects of cannabinoids on the immune response in different pathologies. In addition, we discuss the complexities of using cannabinoid-based treatments in each of these conditions.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1760-1760
Author(s):  
David Nieman ◽  
Arnoud Groen ◽  
Artyom Pugachev ◽  
Andrew Simonson ◽  
Kristine Polley ◽  
...  

Abstract Objectives Proteomics when combined with psychological, nutrition, and performance measures may serve as a useful monitoring system for immune dysfunction, training distress, and exercise-induced muscle damage and exhaustion in athletes. Global proteomics monitoring of an elite adventure athlete (age 33 years) was conducted over a 28-week period that culminated in the successful, unassisted 2-month trek across Antarctica (1500 km). Methods Training distress was monitored weekly using the 19-item, validated Training Distress Scale (TDS). Weekly dried blood spot (DBS) specimens were collected via fingerprick blood drops onto standard blood spot cards. DBS proteins were measured with nano-electrospray ionization liquid chromatography tandem mass spectrometry (nanoLC-MS/MS) in data-independent acquisition (DIA) mode, and 712 proteins were identified and quantified. Results The participant experienced a decrease of 11.4 kg in body mass during the Antarctica trek. The 28-week period was divided into time segments based on TDS scores, and a contrast analysis between weeks 5–8 (low TDS) and weeks 20–23 (high TDS, last month of Antarctica trek) showed that 31 proteins (n = 20 immune related, n = 14 nutrition related with n = 8 in dual roles) were upregulated and 35 (n = 17 immune related) were downregulated. Protein-protein interaction (PPI) networks and gene ontology (GO) biological process analysis supported an increase in plasma lipoprotein particle remodeling, regulation of lipid transport, retinoid metabolic process, and vitamin transport due to high energy intake (7048 kcal/d). PPI networks also supported a dichotomous immune response. GO terms for the upregulated immune proteins showed an increase in regulation of the immune system process, especially inflammation, complement activation, and leukocyte mediated immunity. GO terms for the downregulated immune-related proteins indicated a decrease in several aspects of the overall immune system process including neutrophil degranulation and the antimicrobial humoral response. Conclusions These proteomics data support a dysfunctional immune response in an elite adventure athlete during a sustained period of mental and physical distress, high energy intake, and significant loss of body mass while trekking solo across Antarctica. Funding Sources Standard Process, Inc., Palmyra, WI.


2003 ◽  
Vol 2 (3) ◽  
pp. 183-194 ◽  
Author(s):  
Ludmila Müller ◽  
Graham Pawelec

Currently, the notion of immunosurveillance against tumors is enjoying something of a renaissance. Even if we still refuse to accept that tumors arising in the normal host are unable to trigger an immune response because of the lack of initiation (“danger”) signals, there is no doubt that the immune system can be manipulated experimentally and by implication therapeutically to exert anti-tumor effects. For this activity to be successful, the appropriate cytokine milieu has to be provided, making cytokine manipulation central to immunotherapy. On the other hand, the major hurdle currently preventing successful immunotherapy is the ability of tumors to evolve resistant variants under the pressure of immune selection. Here, too, the cytokine milieu plays an essential role. The purpose of this brief review is to consider the current status of the application of cytokines in facilitating antitumor immunity, as well their role in inhibiting responses to tumors. Clearly, encouraging the former but preventing the latter will be the key to the effective clinical application of cancer immunotherapy.


1969 ◽  
Vol 129 (5) ◽  
pp. 935-951 ◽  
Author(s):  
G. M. Shearer ◽  
G. Cudkowicz

Marrow cell suspensions of unprimed donor mice have been transplanted into X-irradiated syngeneic hosts. 5–46 days later, bone cavities and spleens contained regenerated cells of the immune system which required interaction with thymocytes (from intact donors) and antigen (SRBC) to form antigen-sensitive units (ASU) and to generate mature immunocytes. These cells were capable of differentiating either into direct or indirect hemolytic plaque-forming cells (PFC). The precursors of PFC regenerated earlier than the other cell type necessary for immunocompetence, the antigen-reactive cell (ARC). The latter was not found until 10 or more days after transplantation. Availability of ARC was inferred from PFC responses elicited by grafted mice challenged with SRBC at varying intervals. In a second series of experiments, graded numbers of marrow cells (ranging from 107 to 5 x 107) were transplanted with 5 x 107 or 108 thymocytes into irradiated mice, and SRBC were given 18 hr later. After 9–12 days the recipient spleens contained all or some of the following immunocytes: direct and indirect PFC, and hemagglutinating cluster-forming cells. The frequency of each immune response varied independently of the others, but in relation to the number of marrow cells grafted. This was interpreted to indicate that ASU formed in irradiated mice by interaction of marrow and thymus cells were similar to those of intact mice. In particular, they were specialized for the molecular class (IgM or IgG) and function (lysis or agglutination) of the antibody to be secreted by their descendent immunocytes. Hence, class-differentiation appeared to be conferred upon ASU by their marrow-derived components.


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