scholarly journals C3 AND C4 COMPLEMENT – BIOMARKERS FOR PROGNOSIS OF TREATMENT OF TNF-BLOKERS

2019 ◽  
Vol 32 (2) ◽  
pp. 247-250
Author(s):  
Stanislava Popova ◽  
Mariela Geneva
Keyword(s):  
Immune System ◽  
Complement System ◽  
Inflammatory Diseases ◽  
Adaptive Immune System ◽  
Response Prediction ◽  
The Body ◽  
Control Group ◽  
Phagocytic Cells ◽  
Immune System Activation ◽  
The Complement System

Introduction: The complement system adds antibodies and helps phagocytic cells to destroy pathogens from the body. This is part of a congenital immune system that is not adaptive and does not change over the individual life. However, complement can be "triggered" by the adaptive immune system. The complement system is the main effector of the humoral patr of the immune system. Activation of complement results in opsonization, chemotaxis and cytolysis. Regulation of the complement system can control inflammatory diseases including psoriatic arthritis and vice versa, complement fixation disorders can lead to illness. Treatment with anti-TNF blokers complement activity in patients with inflammatory joint diseases.Objective: To investigate C3, C4 fractions of complement, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and complement the response prediction and monitoring of anti-TNF treatment in patients with psoriatic arthritis.Materials and Methods: 36 patients were included sequentially before treatment with TNF-a-blokers. C3, C4, ESR, CRP were assessed at baseline at 6 and 12 months after initiation of treatment with TNF-α blockers. The activity of the disease is measured by the DARSA disease activity scale, the responses being compared with a control group of persons similar in gender and age. Statistical data processing was performed using the SPSS v25.Results and conclusions: According to the results obtained, C3 and C4 were significantly higher than controls at initiation of treatment (C3 111.3 ± 30.8, C4 91.9 ± 12.4 mg / dl, controls 19.1 ± 8.3 mg / dl, 10.2 ± 5.6 mg / dl p = 0.001, p = 0.001). At 6 and 12 months of follow-up, 76.2% of patients had a reduction in the level of C3 and C4 (p = 0.002, 0.001, respectively). It was found that higher baseline levels of C3 were associated with higher DARSA values at 6 and 12 months.Conclusion: The study of the C3 and C4 complement fractions can be used as biomarkers to estimate the prognosis of TNF-blocker therapy.

scholarly journals Activation of the Complement System in the Lower Genital Tract During Pregnancy and Delivery

2021 ◽  
Vol 11 ◽  
Author(s):  
Sivan Livson ◽  
Hanna Jarva ◽  
Ilkka Kalliala ◽  
A. Inkeri Lokki ◽  
Jenni Heikkinen-Eloranta ◽  
...  
Keyword(s):  
Immune System ◽  
Pregnant Women ◽  
Complement System ◽  
Normal Pregnancy ◽  
Complement C3 ◽  
Control Group ◽  
Activation Level ◽  
Active Labor ◽  
Pregnancy And Delivery ◽  
The Complement System

BackgroundHuman pregnancy alters profoundly the immune system. The local involvement and mechanisms of activation of the complement system in the cervicovaginal milieu during pregnancy and delivery remain unexplored.ObjectivesTo determine whether normal pregnancy and delivery are associated with local activation of complement or changes in the immunoglobulin profile in the cervix.Study DesignThis study was designed to assess IgA, IgG, and complement activation in the cervicovaginal area in three groups of patients: i) 49 pregnant women (week 41+3–42+0) not in active labor, ii) 24 women in active labor (38+4–42+2), and iii) a control group of nonpregnant women (n=23) at child-bearing age. We collected mucosal samples from the lateral fornix of the vagina and external cervix during routine visits and delivery. The Western blot technique was used to detect complement C3 and its activation products. For semiquantitative analysis, the bands of the electrophoresed proteins in gels were digitized on a flatbed photo scanner and analyzed. IgA and IgG were analyzed by Western blotting and quantified by ELISA. One-way ANOVA and Tukey’s Multiple Comparison tests were used for statistical comparisons.ResultsA higher abundance but lower activation level of C3 in both the external cervix (P<0.001) and lateral fornix of the vagina (P<0.001) was observed during delivery (58 ± 22, n= 24) in comparison to the groups of nonpregnant (72 ± 13%; mean ± SD, n=23) and pregnant women (78 ± 22%, n=49). Complement activating IgG was detected in higher abundance than IgA in the cervicovaginal secretions of pregnant women. In a small proportion samples also C3-IgG complexes were detected.ConclusionsOur results reveal an unexpectedly strong activation of the complement system and the presence IgG immunoglobulins in the cervicovaginal area during pregnancy, active labor, and among nonpregnant women. In contrast to the higher amounts of C3 in the cervicovaginal secretions during labor, its activation level was lower. Complement activating IgG was detected in higher concentrations than IgA in the mucosal secretions during pregnancy and labor. Taken together our results imply the presence a locally operating humoral immune system in the cervicovaginal mucosa.

Complement deficiencies

2018 ◽  
Author(s):  
Malini Bhole
Keyword(s):  
Immune System ◽  
Complement System ◽  
Bacterial Infections ◽  
Adaptive Immune System ◽  
Classical Pathway ◽  
Adaptive Immune ◽  
Complement Inhibitors ◽  
Inflammatory Damage ◽  
Form Part ◽  
The Complement System

The complement system comprises a group of heat-labile proteins which form part of the innate immune system. The main physiological functions of the complement system include defence against pyogenic bacterial infections, clearance of immune complexes and products of inflammatory damage, and acting as a bridge between the innate and adaptive immune system. The complement system is regulated by various complement inhibitors (regulatory proteins) that are present in both the classical pathway and the alternate pathway and which regulate and prevent spontaneous activation of the complement system, thereby preventing complement-mediated damage to tissues under normal circumstances. This chapter addresses the clinical features, diagnosis, and management of inherited and acquired deficiencies of complement proteins or inhibitors.

Systemic lupus erythematosus and related disorders

2010 ◽  
pp. 3652-3664 ◽  
Author(s):  
Anisur Rahman ◽  
David A. Isenberg
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune System ◽  
T Lymphocytes ◽  
Complement System ◽  
Lupus Erythematosus ◽  
The Body ◽  
Rheumatic Disorder ◽  
Systemic Lupus ◽  
The Complement System

Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disorder that can present with symptoms in almost any organ or system of the body. It is 10 to 20 times commoner in women than men, and commoner in Afro-Caribbeans than Asians than whites. Aetiology is multifactorial, incorporating genetic, hormonal, and environmental elements. No single abnormality of the immune system can be considered responsible, pathogenesis depending on the interplay of a number of different factors, including autoantibodies, T lymphocytes, cytokines, the complement system, and apoptosis....

Consultation with the Specialist

1996 ◽  
Vol 17 (12) ◽  
pp. 435-440
Author(s):  
Sherilyn Smith ◽  
Marianne T. Sweetser ◽  
Christopher B. Wilson
Keyword(s):  
Immune System ◽  
Life Events ◽  
Host Defense ◽  
Complement System ◽  
Phagocytic Cells ◽  
First Line ◽  
Severe Infections ◽  
Epithelial Barriers ◽  
Exceptional Patient ◽  
The Complement System

Infections are the most frequent illness encountered in children by the pediatrician and, for most patients, represent normal life events. However, the child who has unduly frequent, persistent, or severe infections or who has infection(s) due to microbes that normally are nonpathogenic may represent the exceptional patient who has an immunologic defect. The causative organisms and the age at which the infections begin to occur may provide clues to the nature of the immunologic defect. Components of the Immune System and Their Function in Host Defense The immune system can be divided into two components based on the specificity with which microbes are discriminated from self. The innate or natural immune system is responsible for a rapid, efficient, and nonspecific response to invading microbes. It can be viewed as the first line of defense and is comprised of epithelial barriers, the spleen, phagocytic cells, natural killer (NK) cells, the complement system, and other proteins that aid with opsonization. Abnormalities in this part of the immune system generally predispose to infections from organisms that are ubiquitous and usually of low virulence. The second part of the immune system, the inducible or adaptive portion, is responsible for specific, amplifiable, and long-lived responses to foreign antigens.

Serum immunoglobulins in patients with chronic tonsillitis

1984 ◽  
Vol 98 (12) ◽  
pp. 1213-1216 ◽  
Author(s):  
Harbans Lal ◽  
O. P. Sachdeva ◽  
H. R. Mehta
Keyword(s):  
Immune System ◽  
Mean Value ◽  
The Body ◽  
Antigenic Stimulation ◽  
Chronic Tonsillitis ◽  
Serum Immunoglobulin ◽  
Control Group ◽  
Humoral Immune ◽  
Humoral Immune System ◽  
The Mean

AbstractSerum immunoglobulin (IgG, IgA and IgM) levels were determined in patients with chronic tonsillitis before and one month after tonsillectomy. The preoperative levels of serum IgG, IgA and IgM were significantly higher when compared with the controls. The increase may be due to repeated antigenic stimulation. The post-operative levels for the three immunoglobulins were decreased; however, a significant reduction was observed for IgG only where the mean value was comparable with the control group. The data confirm that tonsillectomy does not disturb the humoral immune system of the body.

scholarly journals Gut Microbiome and Organ Fibrosis

Nutrients ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 352
Author(s):  
Carolina F. F. A. Costa ◽  
Benedita Sampaio-Maia ◽  
Ricardo Araujo ◽  
Diana S. Nascimento ◽  
Joana Ferreira-Gomes ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
Inflammatory Diseases ◽  
Adaptive Immune System ◽  
Organ Damage ◽  
Pathological Process ◽  
The Body ◽  
Intestinal Fibrosis ◽  
Immune Mediated ◽  
Major Player ◽  
Organ Fibrosis

Fibrosis is a pathological process associated with most chronic inflammatory diseases. It is defined by an excessive deposition of extracellular matrix proteins and can affect nearly every tissue and organ system in the body. Fibroproliferative diseases, such as intestinal fibrosis, liver cirrhosis, progressive kidney disease and cardiovascular disease, often lead to severe organ damage and are a leading cause of morbidity and mortality worldwide, for which there are currently no effective therapies available. In the past decade, a growing body of evidence has highlighted the gut microbiome as a major player in the regulation of the innate and adaptive immune system, with severe implications in the pathogenesis of multiple immune-mediated disorders. Gut microbiota dysbiosis has been associated with the development and progression of fibrotic processes in various organs and is predicted to be a potential therapeutic target for fibrosis management. In this review we summarize the state of the art concerning the crosstalk between intestinal microbiota and organ fibrosis, address the relevance of diet in different fibrotic diseases and discuss gut microbiome-targeted therapeutic approaches that are current being explored.

The complement system

2010 ◽  
pp. 213-224
Author(s):  
Marina Botto ◽  
Mark J. Walport
Keyword(s):  
Immune System ◽  
Complement System ◽  
Immune Complexes ◽  
Innate Immune System ◽  
Inflammatory Responses ◽  
Antibody Responses ◽  
Host Defence ◽  
System P ◽  
Dying Cells ◽  
The Complement System

The complement system consists of over 20 distinct proteins and is an essential component of the innate immune system. It is a major effector mechanism of host defence against infection and inflammatory responses, has an important role in the physiological removal of immune complexes and dying cells, and plays an accessory role in the induction of antibody responses....

Corticosteroids increase glutamine utilization in human splanchnic bed

2008 ◽  
Vol 294 (2) ◽  
pp. G548-G553 ◽  
Author(s):  
Ronan Thibault ◽  
Susan Welch ◽  
Nelly Mauras ◽  
Brenda Sager ◽  
Astride Altomare ◽  
...  
Keyword(s):  
De Novo ◽  
Inflammatory Diseases ◽  
The Body ◽  
Glutamine Metabolism ◽  
Severe Illness ◽  
Control Group ◽  
High Dose ◽  
Isotope Tracer ◽  
Healthy Humans ◽  
Tracer Methods

Glutamine is the most abundant amino acid in the body and is extensively taken up in gut and liver in healthy humans. To determine whether glucocorticosteroids alter splanchnic glutamine metabolism, the effect of prednisone was assessed in healthy volunteers using isotope tracer methods. Two groups of healthy adults received 5-h intravenous infusions of l-[1-14C]leucine and l-[2H5]glutamine, along with q. 20 min oral sips of tracer doses of l-[1-13C]glutamine in the fasting state, either 1) at baseline (control group; n = 6) or 2) after a 6-day course of 0.8 mg·kg−1·day−1 prednisone (prednisone group; n = 8). Leucine and glutamine appearance rates (Ra) were determined from plasma [1-14C]ketoisocaproate and [2H5]glutamine, respectively, and leucine and glutamine oxidation from breath 14CO2 and 13CO2, respectively. Splanchnic glutamine extraction was estimated by the fraction of orally administered [13C]glutamine that failed to appear into systemic blood. Prednisone treatment 1) did not affect leucine Ra or leucine oxidation; 2) increased plasma glutamine Ra, mostly owing to enhanced glutamine de novo synthesis (medians ± interquartiles, 412 ± 61 vs. 280 ± 190 μmol·kg−1·h−1, P = 0.003); and 3) increased the fraction of orally administered glutamine undergoing extraction in the splanchnic territory (means ± SE 64 ± 6 vs. 42 ± 12%, P < 0.05), without any change in the fraction of glutamine oxidized (means ± SE, 75 ± 4 vs. 77 ± 4%, not significant). We conclude that high-dose glucocorticosteroids increase in splanchnic bed the glutamine requirements. The role of such changes in patients receiving chronic corticoid treatment for inflammatory diseases or suffering from severe illness remains to be determined.

A Commitment to Lineage

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. SCI-22-SCI-22
Author(s):  
Laurie H. Glimcher ◽  
Vanja Lazarevic ◽  
Joerg Ermann ◽  
Wendy Garrett
Keyword(s):  
Colorectal Cancer ◽  
Immune System ◽  
Molecular Mechanisms ◽  
T Regulatory Cells ◽  
Inflammatory Diseases ◽  
Rectal Adenocarcinoma ◽  
Adaptive Immune System ◽  
T Helper ◽  
T Helper 1

Abstract Abstract SCI-22 The transcription factor T-bet, isolated in our laboratory a decade ago, is a master regulator of Type 1 immunity in cells of both the adaptive and innate immune system. In adaptive immunity, T-bet instigates genetic programs in T helper 1 (Th1) cells and is required for production of the hallmark Th1 cytokine IFNg. It simultaneously represses the differentiation of T helper 2 cells and the profibrotic cytokines IL-13 and TGFb. We have recently determined that T-bet is also a repressor of the Th17 genetic program and have established the molecular mechanisms that underpin that function. T-bet also controls the optimal differentiation and function of the cytolytic CD8 cell, and is required for the development of the natural killer T cell. T-bet deficient animals are largely protected from autoimmune/inflammatory diseases such as multiple sclerosis, systemic lupus, type 1 diabetes and inflammatory arthritis, but are susceptible to type 2 driven diseases such as asthma and scleroderma. An exception to this overall rule is our recent discovery that in the absence of an adaptive immune system, the majority of mice lacking T-bet develop a spontaneous ulcerative colitis that progresses to colonic dysplasia and rectal adenocarcinoma. This colitis and inflammation associated colorectal cancer are MyD88 independent, driven by colitogenic flora and ameliorated by treatment with TNF blockade, antibiotics, and transfer of T regulatory cells. This phenotype maps to the T-bet deficient dendritic cell that drives this pro-inflammatory program; selective over-expression of T-bet in DCs was sufficient to reduce colonic inflammation and prevent the progression to neoplasia. The molecular pathogenesis of TRUC colitis and colitis-associated colorectal (caCRC) shares several key features with human caCRC. This model of colitis and colitis-associated colorectal cancer provides opportunities to further understand host-microbial relationships in inflammation and neoplasia and test preventative and therapeutic strategies pre-clinically. The function and mechanism of action of T-bet in the pathogenesis of immune system driven diseases will be discussed. Disclosures: Glimcher: Merck: Consultancy, Patents & Royalties, Research Funding; Bristol Myers Squibb: Membership on an entity's Board of Directors or advisory committees, Patents & Royalties.

The dynamics of cellular factors of the im-mune system of healthy minks, experimentally infected with eimeriidosis, under specific therapy

2020 ◽  
Vol 2 ◽  
pp. 188-195
Author(s):  
Y. E. Kuznetsov ◽  
◽  
N.V. Kuznetsova ◽  
◽  
Keyword(s):  
Immune System ◽  
T Lymphocytes ◽  
T Lymphocyte ◽  
Defense Mechanism ◽  
The Body ◽  
Control Group ◽  
Treat Ment ◽  
Initial Stage ◽  
Additional Control ◽  
Cellular Factors

The immune response in animals and hu-mans is a biological defense mechanism against negative environmental factors. The immune system is a complex of organs and cells of the body, that reacts (protects) against foreign objects-protozoas and hel-minths. The aim of the study was to investi-gate the dynamics of cellular factors of the immune system of healthy minks, experi-mentally invaded with eimeriidosis against the background of specific immunocorrec-tive therapy. To study the dynamics of T-lymphocytes in the blood of animals, being at the specific immunocorrective therapy, a single-center prospective blind randomized comparative study was conducted in parallel groups. At the initial stage of the study, 56 male minks were isolated from the general population. The first group of clinically healthy animals was the control group. From the second to the sixth groups, animals were spontaneously infected with eimerias and isospores. Animals from the third and fifth groups were treated with coccidiostatic "Stop-coccid". Mink of the 4th and 6th groups received the drug "Ametherm 5%". Minks in the 5th and 6th groups after treat-ment with coccidiostatic were adninistered an immunomodulatory drug of plant origin "Phytodoc-immunostim". The 7th group served as an additional control and received a placebo-water with starch. Thus, the analy-sis of the results of the clinical study showed that the use of specific and immunocorrec-tive therapy has a positive effect on the dy-namics of T-lymphocyte levels in the blood of animals with eimeriidosis. In group 3, where infected minks were treated with "Stop-coccid", the level of T-lymphocytes increased by 35.8% to 41.1%; in the 4th group (administered "Ametherm 5%") the level of T-lymphocytes rose from 35.2% to 42.3%; in the 5th group (administered “Stop-coccid” and immunomodulator) the level of T-lymphocytes changed from 36.5% to 43,0% in the 6-th experimental group (treated "Ametherm 5%" and immunomodu-lator) the level of T-lymphocyte growth from 38.6% to 43.9 per cent.

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