Immune Mechanisms of Depression

2017 ◽  
Author(s):  
Caroline Ménard ◽  
Madeline L. Pfau ◽  
Georgia E. Hodes ◽  
Scott J. Russo
Keyword(s):  
Immune System ◽  
Lupus Erythematosus ◽  
Clinical Findings ◽  
Behavioral Symptoms ◽  
Biological Factors ◽  
Major Depressive ◽  
The Past ◽  
Inflammatory Conditions ◽  
Stress Models ◽  
Pro Inflammatory Cytokines

Mood disorders such as major depressive disorder (MDD) are diagnosed largely based upon behavioral symptoms rather than biological factors. Some have argued that a lack of rigorous biomarker-based diagnosis is the reason why 30%–50% of MDD patients are unresponsive to traditional antidepressant medications. Over the past few decades, MDD has been shown to be highly prevalent in patients suffering from chronic inflammatory conditions, such as lupus erythematosus, multiple sclerosis, etc. Moreover, subgroups of MDD patients have shown consistently higher levels of circulating pro-inflammatory cytokines. Together, these clinical findings suggest that alterations within the immune system might contribute to the behavioral symptoms of MDD. In this chapter, we review the growing literature in both humans with MDD and in rodent stress models of depression that support a role for the immune system in depression.

scholarly journals Prevalencia, causas y tratamiento de la depresión mayor

2017 ◽  
Vol 28 (2) ◽  
Author(s):  
Elsy Arlene Pérez-Padilla ◽  
Víctor Manuel Cervantes-Ramírez ◽  
Nayeli Alejandra Hijuelos-García ◽  
Juan Carlos Pineda-Cortes ◽  
Humberto Salgado-Burgos
Keyword(s):  
Immune System ◽  
Major Depression ◽  
Endocrine System ◽  
Public Health Problem ◽  
Stressful Event ◽  
Structural Level ◽  
Biological Factors ◽  
Major Depressive ◽  
Brain Physiology ◽  
El Sistema

ResumenLa depresión mayor representa un problema de salud pública debido a su alta prevalencia. La etiología de la depresión es compleja, en ella intervienen factores psicosociales, genéticos, y biológicos. Entre los factores psicosociales, se ha observado que los primeros episodios depresivos aparecen después de algún evento estresante, y el estrés que acompaña al primer episodio produce cambios a largo plazo en la fisiología cerebral. Estos cambios de larga duración pueden producir variaciones a nivel estructural y en el funcionamiento de diferentes áreas cerebrales. Entre los factores genéticos que intervienen en la enfermedad depresiva, se ha reportado que alrededor de 200 genes están relacionados con el trastorno depresivo mayor. Dentro de los factores biológicos, existen evidencias de alteraciones a nivel de neurotransmisores, citosinas y hormonas, cuyas acciones inducen modificaciones estructurales y funcionales en el sistema nervioso central, en el sistema inmunológico y en el sistema endocrino, que incrementan el riesgo de padecer la depresión mayor. A pesar de años de estudio, las bases biológicas de la depresión mayor y el mecanismo preciso de la eficacia antidepresiva siguen siendo poco claras. Los objetivos de la presente revisión son el resumir las principales conclusiones de la literatura clínica y experimental en relación con la etiología del trastorno depresivo mayor.Palabras claveDepresión mayor, neurotransmisores, neuroplasticidad, serotonina, norepinefrina, sistema inmune. AbstractMajor depression represents a public health problem due to its high prevalence. The etiology of major depression is complex because involves psychosocial, genetic, and biological factors. Among psychosocial factors, different studies report that the first depressive episode appear after some stressful event and produces long-term changes in brain physiology. These long-lasting changes produce variations at the structural level and in the functioning of different brain areas. Among the genetic factors involved in depressive illness, it has been reported that about 200 genes are related to major depressive disorder. Within the biological factors, there is an evidence of alterations in the level of neurotransmitters, cytosine’s and hormones, whose actions induces structural and functional modifications in the central nervous system, the immune system and the endocrine system, which increases the risk of suffering major depression. Despite years of study, the biological basis of major depression and precise mechanisms of antidepressant efficacy remain unclear. The objective of the present review is to summarize the main conclusions of the clinical and experimental literature regarding to the etiology of major depressive disorder.Key wordsMajor depression, neurotransmitters, neuroplasticity, serotonin, norepinephrine, immune system.

Stable expression ratios of five pyroptosis-inducing cytokines in the spleen and thymus of mice showed potential immune regulation at the organ level

Lupus ◽  
2020 ◽  
Vol 29 (3) ◽  
pp. 290-302
Author(s):  
H Fan ◽  
S Zhang ◽  
N Li ◽  
P Fan ◽  
X Hu ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune System ◽  
Inflammatory Cytokines ◽  
Lupus Erythematosus ◽  
Immune Regulation ◽  
Interleukin 18 ◽  
Systemic Lupus ◽  
Tnf Α ◽  
Organ Level ◽  
Pro Inflammatory Cytokines

Background The immune system is one of the most complex regulatory systems in the body and is essential for the maintenance of homeostasis. Despite recent breakthroughs in immunology, the regulation of the immune system and the etiology of autoimmune diseases such as lupus remain unclear. Systemic lupus erythematosus is a systemic autoimmune disease with abnormally and inconsistently expressed pro-inflammatory cytokines. Pyroptosis is a pro-inflammatory form of programmed cell death that is associated with systemic lupus erythematosus. The thymus and spleen are important immune organs involved in systemic lupus erythematosus. Therefore, this study investigated the difference in expression of pyroptosis-inducing pro-inflammatory cytokines between the spleen and thymus in lupus model mice and in control mice, to describe immune regulation at the organ level. Objective To investigate differences in the expression of pyroptosis-inducing cytokines in the spleen and thymus and to explore immune regulatory networks at the organ level. Methods Two groups of lupus mice and two groups of control mice were utilized for this study. Using the thymus and spleen of experimental animals, mRNA expression levels of five pyroptosis-inducing cytokines (interleukin 1β, interleukin 18, NLRP3, caspase-1 and TNF-α) were determined via quantitative polymerase chain reaction. In addition, tissue distribution of these cytokines was investigated via immunohistochemistry. Results All five pyroptosis-inducing inflammatory cytokines showed higher expression in the spleen than in the thymus ( p < 0.05). Moreover, the spleen/thymus expression ratios of all five pyroptosis-inducing cytokines were not statistically different between the four experimental groups. Expression of all five cytokines exhibited a stable ratio (spleen/thymus ratios). This distinctive stable spleen/thymus ratio was consistent in all four experimental groups. The stable spleen/thymus ratios of the five inflammatory cytokines were as follows: interleukin 1β (2.02 ± 0.9), interleukin 18 (2.07 ± 1.06), caspase-1 (1.93 ± 0.66), NLRP3 (3.14 ± 1.61) and TNF-α (3.16 ± 1.36). Immunohistochemical analysis showed the cytokines were mainly expressed in the red pulp region of the spleen and the medullary region of the thymus, where immune-activated cells aggregated. Conclusion The stable spleen/thymus expression ratios of pyroptosis-inducing cytokines indicated that immune organs exhibit strictly regulated functions to maintain immune homeostasis and adapt to the environment.

Abstract P176: Proportionate Cardiovascular Mortality Patterns Among Patients With Inflammatory Disease In The United States, 1999-2018

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Jacob Groenendyk ◽  
Arjun Sinha ◽  
Adovich Rivera ◽  
Matthew J Feinstein
Keyword(s):  
General Population ◽  
Lupus Erythematosus ◽  
The United States ◽  
Morbidity Burden ◽  
The Past ◽  
Inflammatory Conditions ◽  
Immunodeficiency Virus ◽  
Control And Prevention ◽  
Inflammatory Bowel ◽  
Cvd Mortality

Introduction: Novel therapies have changed the clinical course of several chronic viral and inflammatory conditions over the past two decades. As the morbidity burden of these conditions has changed, competing risks for end-organ diseases including cardiovascular diseases (CVDs) may have likewise evolved. We therefore aimed to investigate changes in the relative burden of CVD mortality over the past two decades across several chronic infectious and inflammatory conditions. Hypothesis: Changes in proportionate CVD-related mortality over the past two decades differ across distinct infectious and inflammatory conditions. Methods: We analyzed 1999-2018 Multiple Causes of Death data from the Centers of Disease Control and Prevention. For several chronic infectious and inflammatory conditions, we analyzed patterns in age-adjusted cardiovascular proportionate mortality, defined as the fraction of deaths in a calendar year with CVD as the underlying cause. We compared age-adjusted proportionate CVD mortality, stratified by sex, for systemic lupus erythematosus (SLE), hepatitis C virus (HCV), human immunodeficiency virus (HIV), inflammatory bowel disease (IBD), psoriasis (PSO), rheumatoid arthritis (RA), and systemic sclerosis (SSc). Results: Proportionate CVD mortality in the general population decreased from 40.9% of 2319606 deaths (1999) to 30.6% of 2778169 deaths (2018), whereas it increased for chronic viral conditions (HCV: 7.0% to 10.2%; HIV: 1.9% to 6.7%) and changed little in SLE (15.3% to 14.4%). Patterns of decreasing proportionate CVD mortality over time were similar for IBD and RA as in the general population. Conclusions: Patterns in proportionate CVD mortality over the past 20 years vary considerably for different chronic infectious and inflammatory conditions. The underlying contributions of infectious and inflammatory burden, off-target effects of therapies, and dynamic changes in competing mortality risk merit further study.

scholarly journals Rhabdomyolysis following Acute Extended-Release Quetiapine Poisoning: A Case Report

2012 ◽  
Vol 2012 ◽  
pp. 1-2 ◽  
Author(s):  
Antonios Liolios ◽  
Othman Sentissi
Keyword(s):  
Case Report ◽  
Extended Release ◽  
Psychiatric Patients ◽  
Case Reports ◽  
Clinical Findings ◽  
Major Depressive ◽  
The Past ◽  
Acute Rhabdomyolysis ◽  
Somatic Comorbidities ◽  
Release Form

Background. During the past few years, there have been a number of case reports concerning rhabdomyolysis following quetiapine poisoning; however, there has been none concerning the medication in its extended-release form.Methods. We present the case report of a 48-year-old man presenting a major depressive disorder and borderline personality disorder, who after voluntary intoxication with 12000 mg of quetiapine extended-release developed signs of acute rhabdomyolysis.Results. The rhabdomyolysis was confirmed by the laboratory and the clinical findings, with elevated levels of creatinine, creatine phosphokinase, and CRP.Discussion. We would like to pinpoint the importance of this complication and our concern of prescribing it for psychiatric patients with chronic somatic comorbidities.

Investigation of the relationship among cortisol, pro-inflammatory cytokines, and the degradation of tryptophan into kynurenine in patients with major depression and suicidal behavior

2021 ◽  
Vol 21 ◽  
Author(s):  
Amel Messaoud ◽  
Mensi Rym ◽  
Douki Wahiba ◽  
Fadoua Neffati ◽  
Mohamed Fadhel Najjar ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Biological Factors ◽  
Biological Mechanisms ◽  
Major Depressive ◽  
Inflammatory Parameters ◽  
Dependent Variables ◽  
Two Parameters ◽  
The Relationship ◽  
Pro Inflammatory Cytokines

Background: The increased degradation of tryptophan (Trp) along the kynurenine (Kyn) pathway due to inflammation and/or activation of the hypothalamic-pituitary–adrenal (HPA) axis has been reported among the biological factors involved in the pathophysiology of major depressive disorder (MDD) and suicide. However, the interaction among these multiple factors is not yet completely clarified. Method: We studied plasma levels of Trp, Kyn, cortisol and proinflammatory cytokines (IL-1, IL-6, IL-12, IL-20) and calculated the ratio Kyn/Trp as an index of the breakdown of Trp into Kyn in 31 suicidal MDD patients and 67 non-suicidal MDD patients. Result: We confirmed that suicidal MDD patients have reduced plasma Trp, higher Kyn and Kyn/Trp ratio, and no difference in cortisol levels than non-suicidal MDD patients. IL-1 and IL-12 levels were significantly higher in suicidal MDD than in non-suicidal MDD (p=0.034 and p=0.023, respectively), whereas Il-6 and IL-20 levels were equal in the two groups. The Kyn/Trp ratio was positively correlated with a pro-inflammatory cytokines index (r=0.309, p=0.002) and cortisol (r=0.368, p=0.001). Notably, the variance in the Kyn/Trp ratio explained by the model, including both cortisol and inflammatory parameters as dependent variables, substantially improved compared with the models in which the two parameters were considered separately. Conclusion: These findings show that both cortisol and proinflammatory cytokines are involved in the enhanced breakdown of Trp into Kyn occurring in suicidal MDD patients, thus adding new knowledge on the biological mechanisms leading to the activation of the Kyn pathway in MDD and suicide.

scholarly journals Molecular Pathogenesis of Hodgkin Lymphoma: Past, Present, Future

2020 ◽  
Vol 21 (18) ◽  
pp. 6623 ◽  
Author(s):  
Marc Bienz ◽  
Salima Ramdani ◽  
Hans Knecht
Keyword(s):  
Immune System ◽  
Targeted Therapy ◽  
Signaling Pathways ◽  
Hodgkin Lymphoma ◽  
Genetic Instability ◽  
Host Immune System ◽  
Cellular Interactions ◽  
Classical Hodgkin Lymphoma ◽  
The Past

Our understanding of the tumorigenesis of classical Hodgkin lymphoma (cHL) and the formation of Reed–Sternberg cells (RS-cells) has evolved drastically in the last decades. More recently, a better characterization of the signaling pathways and the cellular interactions at play have paved the way for new targeted therapy in the hopes of improving outcomes. However, important gaps in knowledge remain that may hold the key for significant changes of paradigm in this lymphoma. Here, we discuss the past, present, and future of cHL, and review in detail the more recent discoveries pertaining to genetic instability, anti-apoptotic signaling pathways, the tumoral microenvironment, and host-immune system evasion in cHL.

scholarly journals Nexus between COVID-19 and periodontal disease

2021 ◽  
Vol 49 (3) ◽  
pp. 030006052110026
Author(s):  
Kanchana Sukumar ◽  
Anupama Tadepalli
Keyword(s):  
Periodontal Disease ◽  
Host Cells ◽  
Multifactorial Disease ◽  
Tissue Destruction ◽  
The Past ◽  
Appropriate Care ◽  
Bacterial Stimulation ◽  
Plaque Control ◽  
Disease Understanding ◽  
Pro Inflammatory Cytokines

Over the past several decades, studies have demonstrated the existence of bi-directional relationships between periodontal disease and systemic conditions. Periodontitis is a polymicrobial and multifactorial disease involving both host and environmental factors. Tissue destruction is primarily associated with hyperresponsiveness of the host resulting in release of inflammatory mediators. Pro-inflammatory cytokines play a major role in bacterial stimulation and tissue destruction. In addition, these cytokines are thought to underlie the associations between periodontitis and systemic conditions. Current research suggests that increased release of cytokines from host cells, referred to as the cytokine storm, is associated with disease progression in patients with coronavirus disease 2019 (COVID-19). An intersection between periodontitis and pulmonary disease is biologically plausible. Hence, we reviewed the evidence linking COVID-19, cytokines, and periodontal disease. Plaque control is essential to prevent exchange of bacteria between the mouth and the lungs, reducing the risk of lung disease. Understanding these associations may help identify individuals at high risk and deliver appropriate care at early stages.

scholarly journals P051 Symptoms of COVID-19 and anxiety levels in adult patients receiving b-and ts-DMARDS using an online reporting system

Rheumatology ◽  
2021 ◽  
Vol 60 (Supplement_1) ◽  
Author(s):  
May Nwe Lwin ◽  
Christopher Holroyd ◽  
Dinny Wallis ◽  
Saul Faust ◽  
Hans De Graaf ◽  
...  
Keyword(s):  
Lupus Erythematosus ◽  
Joint Pain ◽  
Connective Tissue Diseases ◽  
Anxiety Score ◽  
Online Portal ◽  
Inflammatory Conditions ◽  
Advanced Therapy ◽  
Number Of Patients ◽  
Patient Reported ◽  
Anxiety Levels

Abstract Background/Aims  The coronavirus disease-2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for over 120,000 UK deaths. Those with chronic inflammatory conditions or receiving immunosuppressive medications are at higher risk of COVID-19 than the general population. As a result, rheumatology patients taking b- or ts-DMARDs were advised to shield. We planned to observe COVID-19 related symptoms and anxiety levels reported by rheumatology patients during the pandemic. Methods  From April 2020, 1,004 rheumatology patients from an advanced therapy database were invited to participate in the adult ImmunoCOVID study to collect daily symptoms (fever, cough, shortness of breath (SOB), sore throat, blocked nose, red-eye, headache, fatigue, joint pain, muscle pain, chills, nausea, diarrhoea and vomiting, loss of senses) and anxiety level using an online portal. Loss of senses were not recorded until week 7 as these were not officially recognized at the pandemic onset. Results  153 patients (rheumatoid arthritis, n = 75, psoriatic arthritis, n = 28, Axial spondyloarthropathy, n = 24, systemic lupus erythematosus, n = 2 and other connective tissue diseases, n = 24) consented and participated. By week 25, 142 patients remained. Among those, 36.57% (±6.09%) (average (±SD)) reported no symptoms over the 25 week period. The main symptoms reported were joint pain (mean=47.94%) followed by fatigue (27.17%). Few patients reported fever (0.94%), cough (8.34%), SOB (4.53%), or loss of senses (1.11%) with more symptoms reported during the first 8 weeks (April/May 2020) and another increase in September/October 2020. The anxiety score (pragmatic 10-point scale) mean (±SD) was 5.60 (±0.34) and remained elevated throughout the study though higher when lockdown began. Conclusion  During the first peak of SARS-CoV-2, the number of patients reporting COVID-19 symptoms appeared high and was associated with high levels of anxiety. As only a small number have been swab-tested, this may suggest that larger numbers of untested individuals have had COVID-19 with mild symptoms. Features of inflammatory rheumatic illnesses may mimic COVID-19 symptoms and create diagnostic difficulty (joint pain and fatigue) whilst anxiety may lead to over-reporting of symptoms in the absence of infection. The key symptoms of fever, cough and SOB were less common and may be most reliable. Disclosure  M. Lwin: None. C. Holroyd: None. D. Wallis: None. S. Faust: None. H. De Graaf: None. C.J. Edwards: Honoraria; Abbvie, Biogen, BMS, Celgene, Fresenius, GSK, Janssen, Lilly, Mundipharma, Pfizer, Roche, Sanofi, UCB. Member of speakers’ bureau; Abbvie, Biogen, BMS, Celgene, Janssen, Lilly, Sanofi, Pfizer, Roche. Grants/research support; Abbvie, Biogen, Pfizer. P051 Table 1:patient reported symptoms and anxiety score from immunoCOVID studyWeek & (number of participants)Fever (%)Cough (%)SOB (%)Joint pain (%)Fatigue (%)Loss of senses (%)No symptoms (%)Tested (n)Test positive (n)Anxiety score1 (26)3.857.6911.5446.1530.77NA30.77006.312 (42)2.3311.639.3052.3834.88NA28.57005.833 (69)1.4514.494.3552.1737.68NA23.19415.884 (92)1.0911.966.5254.3531.52NA27.17206.225 (110)0.0011.716.3145.9533.33NA30.00006.156 (108)0.0010.193.7050.0026.85NA34.26205.747 (119)0.8410.084.2049.5828.57NA34.45205.938 (120)0.007.505.0051.6734.170.8329.17305.629 (124)0.817.263.2352.4229.840.8136.29405.6410 (118)0.008.473.3948.3129.660.8534.75205.2811 (116)0.858.476.7849.1529.661.6933.62305.6512 (131)0.006.114.5856.4926.720.7635.11205.4513 (110)0.916.362.7350.0029.091.8242.73105.4414 (121)0.837.442.4847.1125.620.8339.67805.2815 (100)1.007.003.0046.0023.001.0041.00405.4816 (114)0.887.893.5139.4725.441.7542.98905.2717 (105)0.008.573.8144.7622.860.9543.81425.1018 (107)0.006.543.7443.9319.630.9343.93405.3019 (99)0.005.052.0240.4019.191.0145.45505.0820 (110)0.914.552.7350.9124.550.9139.09NA0Missing data21 (106)0.946.602.8350.0020.750.9439.62405.2822 (104)2.889.626.7349.0430.770.9635.58305.5023 (106)1.897.553.7742.4526.420.9436.79805.8924 (108)0.938.332.7844.4422.220.9341.67605.6125 (94)1.067.454.2641.4915.962.1344.68605.49Average0.948.344.5347.9427.171.1136.575.60SD0.972.312.254.395.350.426.090.34Weekly data are the average of daily reported symptoms and anxiety levels.

scholarly journals Mesenchymal stem cells and oncolytic viruses: joining forces against cancer

2021 ◽  
Vol 9 (2) ◽  
pp. e001684
Author(s):  
Rafael Moreno
Keyword(s):  
Stem Cells ◽  
Clinical Trials ◽  
Mesenchymal Stem Cells ◽  
Immune System ◽  
Oncolytic Viruses ◽  
Immunogenic Cell Death ◽  
The Past ◽  
Physical Barriers ◽  
Immunogenic Properties ◽  
New Strategies

The development of oncolytic viruses (OVs) has increased significantly in the past 20 years, with many candidates entering clinical trials and three of them receiving approval for some indications. Recently, OVs have also gathered interest as candidates to use in combination with immunotherapies for cancer due to their immunogenic properties, which include immunogenic cell death and the possibility to carry therapeutic transgenes in their genomes. OVs transform non-immunogenic ‘cold’ tumors into inflamed immunogenic ‘hot’ tumors, where immunotherapies show the highest efficacy. However, in monotherapy or in combination with immunotherapy, OVs face numerous challenges that limit their successful application, in particular upon systemic administration, such as liver sequestration, neutralizing interactions in blood, physical barriers to infection, and fast clearance by the immune system. In this regard, the use of mesenchymal stem cells (MSCs) as cells carrier for OV delivery addresses many of these obstacles acting as virus carriers and factories, expressing additional transgenes, and modulating the immune system. Here, I review the current progress of OVs-loaded MSCs in cancer, focusing on their interaction with the immune system, and discuss new strategies to improve their therapeutic efficacy.

scholarly journals O21 The incidence of COVID-19 among children with rheumatic diseases receiving biological agents

Rheumatology ◽  
2021 ◽  
Vol 60 (Supplement_1) ◽  
Author(s):  
Nadezhda Tsurikova ◽  
Elena Ligostaeva ◽  
Vadim Avdeenko ◽  
Nataliya Kobzeva ◽  
Irina Tsiganok ◽  
...  
Keyword(s):  
Rheumatic Diseases ◽  
Lupus Erythematosus ◽  
Biological Agents ◽  
Tnf Receptor ◽  
The Past ◽  
Different Types ◽  
Mediterranean Fever ◽  
Positive Results ◽  
Single Center Observational Study

Abstract Background/Aims  During the COVID-19 pandemic, analysis of the incidence of COVID-19 among patients suffering from rheumatic diseases and receiving therapy with biological agents remains relevant. Methods  This single-center observational study included 118 children suffering from various rheumatic diseases and receiving therapy with anti-rheumatic drugs and biological agents. In this research, we analyzed the incidence of CIVID-19 and the frequency of documented contact with SARS-CoV-2 in the period from 01.03.2020 to 11.10.2020 (32 weeks). The results were analyzed using descriptive statistics. Results  Among 118 children, there were 28 (24%) boys and 90 (76%) girls, average age 10.3±4.2. 104 (88.2%) patients had different types of juvenile idiopathic arthritis (JIA), 2 (1.6%) children had systemic lupus erythematosus (SLE), 2 (1.6%) patients had juvenile dermatomyositis (JDM), 1 (1%) child had ANCA-associated vasculitis, 6 (5%) patients had familial Mediterranean fever (FMF), 2 (1.6%) children had deficiency of adenosine deaminase 2 (DADA2), 1 (1%) child had TNF receptor-associated periodic syndrome (TRAPS). In this group of patients 94 (79%) patients were treated with methotrexate, 1 (1%) - azathioprine, 3 (2%) patients received hydroxychloroquine, 6(5%) - mycophenolate mofetil, 4 (3%) - sulfasalazine, 14(11%) children received prednisone, 6(5%) - cyclosporine A. All children included in this study received biological agents for more than 1 year, the distribution of biological agents among patients was as follows: 41(34%) - etanercept, 33(28%) - adalimumab, 24 (20%) - tocilizumab, 7 (6%) - canakinumab, 3 (2%) - abatacept, 4 (3%) - golimumab, 6 (5%) - rituximab. Out of 118 children, 4 (3%) patients had flu-like symptoms and positive results of PCR tests for COVID-19 (1 patient was treated with etanercept, 1 - adalimumab, 1 - tocilizumab, 1 - rituximab), none of the patients had signs of SARS-CoV-2 pneumonia. 10 (8%) patients had documented contact with COVID-19: among this patients 2 children had flu-like symptoms, positive results of PCR tests and absence of COVID-19 pneumonia (one of this patient was treated with adalimumab, another one - with rituximab), one more patient was treated with tocilizumab and had positive PCR test without any symptoms of COVID-19; other 7 children had negative PCR tests and didn’t have any signs of COVID-19. Conclusion  Among our patients with various rheumatic diseases treated with biological agents there were no registered severe cases of COVID-19. Over the past period (32 weeks of follow-up) 3% of children with COVID-19 were identified and 8% patients had documented contact with COVID-19, but we suppose it is too early to make conclusions about the degree and severity of COVID-19 among children suffering from rheumatic diseases and receiving various biological agents. Further follow-up is needed to better understand the risk and impact of COVID-19 among children with rheumatic diseases and receiving therapy with biological agents. Disclosure  N. Tsurikova: None. E. Ligostaeva: None. V. Avdeenko: None. N. Kobzeva: None. I. Tsiganok: None. K. Skorobogatova: None. A. Motkina: None.

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