Результаты поиска

Interleukin-24 in type 2 immune diseases.

Interleukin (IL)-24, a member of the IL-20 cytokine family, is secreted by multiple cell types, such as immune cells (T cells, B cells, NK cells, macrophages), and non-immune cells (epithelial cells and fibroblasts). IL-24 and its downstream signaling pathways mediate vital biological processes, including processes governing cell growth, fate determination, cell death, and inflammation, albeit with effects that are context-dependent across disease states. In this review, we present comprehensive summary and recent breakthroughs in IL-24 characterization and its emerging pathogenic functions in

Interleukin-23 Inhibitors in Inflammatory Bowel Disease.

Selective inhibition of interleukin-23 (IL-23) has emerged as a highly effective therapeutic strategy in inflammatory bowel disease, targeting a central pathway of chronic intestinal inflammation while preserving host defense mechanisms. Across phase II and phase III randomized controlled trials, risankizumab, mirikizumab, and guselkumab consistently demonstrated robust efficacy in both ulcerative colitis and Crohn's disease, achieving clinical remission rates approaching 40-50% in ulcerative colitis and exceeding 50% in Crohn's disease during maintenance, with parallel improvements in endosco

Interleukin-31: A Pro-inflammatory Oriented Cytokine.

Type 2 immunity is represented by T helper 2 (Th2) lymphocytes and the cytokines produced downstream (Interleukin (IL)-4, IL-13, IL-31). They are increasingly recognized as pivotal mediators in the pathogenesis of immune-mediated dermatological conditions such as atopic dermatitis (AD) and psoriasis (Pso). In these disorders, they initiate and amplify immunological signaling cascades, promote cutaneous inflammation, and contribute to the induction of pruritus. In this context, IL-33 and IL-31 would be believed to be intrinsically linked and related to the acuity of the disease. The presence of

Dynamics and variegation in the Treg response to Interleukin-2.

Interleukin-2 (IL2) is the key trophic factor for T regulatory (Treg) cells, controlling their differentiation and homeostasis. To understand how temporally regulated responses to IL2 unfold in Tregs, we performed fine time-course analyses, at population and single-cell levels, of changes in chromatin architecture and mRNAs induced by IL2 in Tregs in vivo. The data revealed responses that were largely uniform in rTreg, but diverse among aTregs, matching different STAT5 signal transduction efficiency. Individual Tregs displayed divergences in the preponderance of changes that may be attributed

Expression of interleukin-4 in schistosomiasis is influenced by age.

BACKGROUND: Schistosomiasis, a Neglected Tropical Disease (NTD), remains a significant public health issue, particularly in sub-Saharan Africa. Despite various interventions, the disease persists, with a considerable burden on affected populations. This study aimed to characterize the hematological and immunological profiles associated with Schistosoma infection in pediatric and adult populations in Mulobezi district of Zambia. METHODS: This was a cross-sectional study, which included participants aged 5-55 years, carried out in Mulobezi District in the Western Province of Zambia. The sample

The role of Interleukin-22 in severe acute pancreatitis.

Severe acute pancreatitis (SAP) begins with premature activation of enzymes, promoted by the immune system, triggering a potential systemic inflammatory response that leads to organ failure with increased mortality and a bleak prognosis. Interleukin-22 (IL-22) is a cytokine that may have a significant role in SAP. IL-22, a member of the IL-10 cytokine family, has garnered growing interest owing to its potential tissue-protective properties. Recently, emerging research has revealed its specific effects on pancreatic diseases, particularly SAP. This paper provides a review of the latest knowledg

Variants at the Interleukin 1 Gene Locus and Pericarditis.

IMPORTANCE: Recurrent pericarditis is a treatment challenge and often a debilitating condition. Drugs inhibiting interleukin 1 cytokines are a promising new treatment option, but their use is based on scarce biological evidence and clinical trials of modest sizes, and the contributions of innate and adaptive immune processes to the pathophysiology are incompletely understood. OBJECTIVE: To use human genomics, transcriptomics, and proteomics to shed light on the pathogenesis of pericarditis. DESIGN, SETTING, AND PARTICIPANTS: This was a meta-analysis of genome-wide association studies of peri

Interleukin-17 Inhibitors in the Treatment of Hidradenitis Suppurativa.

Hidradenitis suppurativa (HS) is a chronic, debilitating, inflammatory dermatosis that significantly impacts patients' quality of life, primarily manifesting as inflammatory nodules, abscesses, and tunnels. The pathogenesis of HS is not fully understood and appears to be multifactorial, involving genetic, immunological, and endocrinological factors, as well as dysbiosis of skin microbiota. Increasing evidence highlights the role of the interleukin (IL)-17 pathway in the inflammatory process and pathogenesis of HS. Consequently, IL-17 inhibitors have emerged as a promising alternative to curren

The role of interleukin-36 in health and disease states.

The interleukin (IL)-1 superfamily upregulates immune responses and maintains homeostasis between the innate and adaptive immune systems. Within the IL-1 superfamily, IL-36 plays a pivotal role in both innate and adaptive immune responses. Of the four IL-36 isoforms, three have agonist activity (IL-36α, IL-36β, IL-36γ) and the fourth has antagonist activity (IL-36 receptor antagonist [IL-36Ra]). All IL-36 isoforms bind to the IL-36 receptor (IL-36R). Binding of IL-36α/β/γ to the IL-36R recruits the IL-1 receptor accessory protein (IL-1RAcP) and activates downstream signalling pathways mediated

" Interleukin " ( < < Интерлейкин > > ) в связи с заболеваниями, обусловленными иммунной средой: обновленный обзор.

Иммунная система состоит из различных регуляторов и проводников, которые вызывают иммунную реакцию на различные нападения на тело. Патогенез аутоиммунных заболеваний вызван дерегулированным выражением цитокина, основного регулятора иммунной системы. Среди цитокинов интерлейкины оказывают значительное влияние на иммунные заболевания. Эти интерлеуцины инициируют иммунную реакцию на здоровые и нормальные клетки организма, что приводит к иммуномедицинскому заболеванию. Основными интерлейкинами в этом отношении являются IL-1, IL-3, IL-4, IL-6, IL-10 и IL-12, которые вызывают такие иммунные реакции,

Совпадение в аннотации оригинала
The immune system comprises various regulators and effectors that elicit immune responses against various attacks on the body. The pathogenesis of autoimmune diseases is derived from the deregulated expression of cytokines, the major regulators of the immune system. Among cytokines, interleukins have a major influence on immune-mediated diseases. These inter…

The Important Role of Interleukin-2 in COVID-19.

There is controversial literature about the effects of the interleukin-2 (IL-2) cytokine family in COVID-19 pathogenesis and immunity. So we aimed to identify the potential in the role of the IL-2 family in COVID-19. A narrative review search was done through online databases, including PubMed, Scopus, and Web of Science. The search deadline was up to December 2022. We applied no time limits for the searching strategy. After retrieving articles from the databases, the authors summarized the data into two data extraction tables. The first data extraction table described the changes in the IL-2

Rethinking Oncologic Treatment Strategies with Interleukin-2.

High-dose recombinant human IL-2 (rhIL-2, aldesleukin) emerged as an important treatment option for selected patients with metastatic melanoma and metastatic renal cell carcinoma, producing durable and long-lasting antitumor responses in a small fraction of patients and heralding the potential of cancer immunotherapy. However, the adoption of high-dose rhIL-2 has been restricted by its severe treatment-related adverse event (TRAE) profile, which necessitates highly experienced clinical providers familiar with rhIL-2 administration and readily accessible critical care medicine support. Given th

The Role of the Interleukin-1 Family in Complications of Prematurity.

Preterm birth is a major contributor to neonatal morbidity and mortality. Complications of prematurity such as bronchopulmonary dysplasia (BPD, affecting the lung), pulmonary hypertension associated with BPD (BPD-PH, heart), white matter injury (WMI, brain), retinopathy of prematurity (ROP, eyes), necrotizing enterocolitis (NEC, gut) and sepsis are among the major causes of long-term morbidity in infants born prematurely. Though the origins are multifactorial, inflammation and in particular the imbalance of pro- and anti-inflammatory mediators is now recognized as a key driver of the pathophys

Role of Interleukin-36 in inflammatory joint diseases.

Interleukin (IL)-36 is a family of cytokines that belongs to the larger IL-1 superfamily. IL-36 agonist/antagonist binds to the interleukin-36 receptor involving in physiological inflammation regulation and pathogenesis of many inflammatory diseases. In inflammatory joint diseases, the expression of IL-36 changes, and some studies have initially explored the role of IL-36 in these diseases. In psoriatic arthritis, IL-36 signal mediates plasma cell and fibroblast-like synoviocyte crosstalk presenting IL-36 agonist/antagonist imbalance. In rheumatoid arthritis, IL-36 agonists induce fibroblast-l

Mechanistic insight of interleukin-9 induced osteoclastogenesis.

Interleukin (IL)-9 is an emerging player in the pathogenesis of various chronic inflammatory diseases including bone disorders like rheumatoid arthritis (RA) and psoriatic arthritis. Recently, IL-9 was shown to enhance the osteoclast formation and their function in RA. However, the mechanisms by which IL-9 influences osteoclastogenesis are not known. Therefore, in this study we aimed to unravel the direct and indirect ways by which IL-9 can influence osteoclast formation. We used mouse bone marrow precursor cells for checking the effect of IL-9 on osteoclast differentiation and its function. N

Interleukin 6: at the interface of human health and disease.

Interleukin 6 (IL-6) is a pleiotropic cytokine executing a diverse number of functions, ranging from its effects on acute phase reactant pathways, B and T lymphocytes, blood brain barrier permeability, synovial inflammation, hematopoiesis, and embryonic development. This cytokine empowers the transition between innate and adaptive immune responses and helps recruit macrophages and lymphocytes to the sites of injury or infection. Given that IL-6 is involved both in the immune homeostasis and pathogenesis of several autoimmune diseases, research into therapeutic modulation of IL-6 axis resulted

Interleukin-37 is involved in the immunopathogenesis of infectious mononucleosis.

BACKGROUND: Multiple immunopathological responses to viruses are observed in infectious mononucleosis (IM), a manifestation of primary infection with Epstein-Barr virus (EBV). Protective effects of the negative immunoregulatory molecule interleukin-37 (IL-37) have been observed in various bacterial and viral infections. However, the function of IL-37 in IM remains unknown. METHODS: Flow cytometry and enzyme-linked immunosorbent assay (ELISA) were used to determine the expression of IL-37 in the peripheral blood of patients diagnosed with IM, and the variation of lymphocyte subsets. Furthermor

Interleukin-6 inhibition in the treatment of autoinflammatory diseases.

Autoinflammatory diseases are characterized by abnormalities that prevent innate immune cells from producing autoantibodies. While interleukin (IL)-6 is not directly associated with inflammasomes, like IL-1β or IL-18, it plays an important role in the pathogenesis of autoinflammatory diseases. Studies of autoinflammatory diseases, such as familial Mediterranean fever, cryopyrin-associated periodic syndrome, and tumor necrosis factor receptor-associated periodic syndrome, have shown IL-6 to be a promising therapeutic target. It has also been suggested that inhibition of IL-6 may have a therapeu