scholarly journals The Role of Innate and Adaptive Immune Cells in the Pathogenesis and Development of the Inflammatory Response in Ulcerative Colitis

2022 ◽  
Vol 11 (2) ◽  
pp. 400
Author(s):  
Aleksandra Kałużna ◽  
Paweł Olczyk ◽  
Katarzyna Komosińska-Vassev
Keyword(s):  
Ulcerative Colitis ◽  
Immune Response ◽  
Immune Cells ◽  
Chronic Inflammatory Disease ◽  
Lymphoid Cells ◽  
Cytotoxic Lymphocytes ◽  
Adaptive Immune ◽  
Adaptive Immune Cells ◽  
Th17 Lymphocytes ◽  
The Impact

Ulcerative colitis (UC) is a chronic inflammatory disease with an underlying excessive immune response directed against resident microbiota and/or dietary antigens. Both innate and adaptive immune cells play a crucial role in the pathogenesis of UC. In the case of innate immune response cells, neutrophils, dendritic cells, macrophages have a crucial impact on the development of the disease, as well as innate lymphoid cells, which have received a particular attention in recent years. On the other hand, mechanisms of the adaptive immune response involve cells such as: cytotoxic lymphocytes, regulatory lymphocytes Treg, or helper lymphocytes Th–Th2, Th9, Th17, Th22, among which significant discoveries about Th9 and Th17 lymphocytes have been made in recent years. Due to the presence of antibodies directed against resident microbiota or one’s own tissues, the influence of B lymphocytes on the development of UC is also highlighted. Additionally, the impact of cytokines on shaping the immune response as well as sustaining inflammation seems to be crucial. This review briefly describes the current state of knowledge about the involvement of the innate and adaptive immune systems in the pathogenesis of UC. The review is based on personal selection of literature that were retrieved by a selective search in PubMed using the terms “ulcerative colitis” and “pathogenesis of ulcerative colitis”. It included systematic reviews, meta-analyses and clinical trials. Our knowledge of the involvement of the immune system in the pathophysiology of IBD has advanced rapidly over the last two decades, leading to the development of several immune-targeted treatments with a biological source, known as biologic agents.

scholarly journals Immune Response to SARS-CoV-2 Infection

2020 ◽  
Vol 03 (10) ◽  
Author(s):  
Dr. Ahmed Al-Shukaili ◽  
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Severe Acute Respiratory Syndrome ◽  
Global Health ◽  
Immune Cells ◽  
Current Knowledge ◽  
Adaptive Immune ◽  
Proinflammatory Mediators ◽  
Adaptive Immune Cells ◽  
New Type

In December 2019 a new type of coronaviruses appeared in China and named Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the disease associated with this virus is called Coronavirus Disease 2019 or COVID-19. Currently, COVID19 is the main global health threat. In this review, we focus in the current knowledge of immune response to SARS-CoV-2. Dysregulation of immune system, such as elevation levels of proinflammatory mediators and their roles in disease progression and pathogenesis as well as imbalance between innate and adaptive immune cells, are discussed in this review.

scholarly journals Zika virus encephalitis in immunocompetent mice is dominated by innate immune cells and does not require T or B cells

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Emina Hayashida ◽  
Zheng Lung Ling ◽  
Thomas M. Ashhurst ◽  
Barney Viengkhou ◽  
So Ri Jung ◽  
...  
Keyword(s):  
Immune Response ◽  
B Cells ◽  
Immune Cells ◽  
Zika Virus ◽  
Innate Immune ◽  
Wild Type ◽  
Adaptive Immune ◽  
Intracranial Infection ◽  
Adaptive Immune Cells ◽  
Immunocompetent Mice

Abstract Background Until the end of the twentieth century, Zika virus (ZIKV) was thought to cause a mostly mild, self-limiting disease in humans. However, as the geographic distribution of ZIKV has shifted, so too has its pathogenicity. Modern-day ZIKV infection is now known to cause encephalitis, acute disseminated encephalomyelitis, and Guillain-Barré syndrome in otherwise healthy adults. Nevertheless, the underlying pathogenetic mechanisms responsible for this shift in virulence remain unclear. Methods Here, we investigated the contribution of the innate versus the adaptive immune response using a new mouse model involving intracranial infection of adult immunocompetent mice with a moderately low dose of ZIKV MR766. To determine the contribution of type I interferons (IFN-Is) and adaptive immune cells, we also studied mice deficient for the IFN-I receptor 1 (Ifnar1−/−) and recombination-activating gene 1 (Rag1−/−). Results We show that intracranial infection with ZIKV resulted in lethal encephalitis. In wild-type mice, ZIKV remained restricted predominantly to the central nervous system (CNS) and infected neurons, whereas astrocytes and microglia were spared. Histological and molecular analysis revealed prominent activation of resident microglia and infiltrating monocytes that were accompanied by an expression of pro-inflammatory cytokines. The disease was independent of T and B cells. Importantly, unlike peripheral infection, IFN-Is modulated but did not protect from infection and lethal disease. Lack of IFN-I signaling resulted in spread of the virus, generalized inflammatory changes, and accelerated disease onset. Conclusions Using intracranial infection of immunocompetent wild-type mice with ZIKV, we demonstrate that in contrast to the peripheral immune system, the CNS is susceptible to infection and responds to ZIKV by initiating an antiviral immune response. This response is dominated by resident microglia and infiltrating monocytes and macrophages but does not require T or B cells. Unlike in the periphery, IFN-Is in the CNS cannot prevent the establishment of infection. Our findings show that ZIKV encephalitis in mice is dependent on the innate immune response, and adaptive immune cells play at most a minor role in disease pathogenesis.

scholarly journals A comprehensive logic-based model of the human immune system to study the dynamics responses to mono- and coinfections

2020 ◽  
Author(s):  
Bhanwar Lal Puniya ◽  
Robert Moore ◽  
Akram Mohammed ◽  
Rada Amin ◽  
Alyssa La Fleur ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
Immune Cells ◽  
Computational Models ◽  
Single Infection ◽  
Human Immune System ◽  
Adaptive Immune ◽  
Adaptive Immune Cells ◽  
Human Immune

AbstractThe human immune system, which protects against pathogens and diseases, is a complex network of cells and molecules. The effects of complex dynamical interactions of pathogens and immune cells on the immune response can be studied using computational models. However, a model of the entire immune system is still lacking. Here, we developed a comprehensive computational model that integrates innate and adaptive immune cells, cytokines, immunoglobulins, and nine common pathogens from different classes of virus, bacteria, parasites, and fungi. This model was used to investigate the dynamics of the immune system under two scenarios: (1) single infection with pathogens, and (2) various medically relevant pathogen coinfections. In coinfections, we found that the order of infecting pathogens has a significant impact on the dynamics of cytokines and immunoglobulins. Thus, our model provides a tool to simulate immune responses under different dosage of pathogens and their combinations, which can be further extended and used as a tool for drug discovery and immunotherapy. Furthermore, the model provides a comprehensive and simulatable blueprint of the human immune system as a result of the synthesis of the vast knowledge about the network-like interactions of various components of the system.

scholarly journals The Problem of Antigen Affinity Discrimination in B-Cell Immunology

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Subhadip Raychaudhuri
Keyword(s):  
Immune Response ◽  
B Cell ◽  
Immune Cells ◽  
Molecular Mechanisms ◽  
Vaccine Development ◽  
Single Cells ◽  
Affinity Maturation ◽  
Adaptive Immune ◽  
Adaptive Immune Cells ◽  
Cell Affinity

B and T lymphocytes activate the humoral and cellular arms of the adaptive immune system. The adaptive strategy works because receptors of adaptive immune cells can mount an immune response based on their affinity for antigens. Thus, affinity discrimination is central to adaptive immunity and has important biomedical ramifications. Due to its intricate connection to the affinity maturation process, affinity discrimination has a special significance in B-cell-mediated immune response. The role of affinity-matured high-affinity antibodies is increasingly recognized in vaccine development. In this paper, we discuss the recent progress made in mathematical and computational studies to explore the cellular and molecular mechanisms of B-cell affinity discrimination. Formation of B-cell receptor (BCR) oligomers and BCR-lipid rafts, upon antigenic stimulation, emerge to be key factors in B-cell affinity discrimination (at the level of single cells). It also provides a new way of thinking about kinetic proofreading and serial triggering, concepts that have been widely utilized to understand affinity discrimination in adaptive immune cells. Potential future applications of mathematical and computational modeling of affinity discrimination are discussed in the context of autoimmune disorders and vaccine design.

scholarly journals The impact of body mass index on adaptive immune cells in the human bone marrow

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Luca Pangrazzi ◽  
Erin Naismith ◽  
Carina Miggitsch ◽  
Jose’ Antonio Carmona Arana ◽  
Michael Keller ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Bone Marrow ◽  
Body Mass ◽  
Immune Cells ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Adaptive Immune ◽  
Adaptive Immune Cells ◽  
The Impact

scholarly journals Heterogeneity and clonal relationships of adaptive immune cells in ulcerative colitis revealed by single-cell analyses

2020 ◽  
Vol 5 (50) ◽  
pp. eabb4432 ◽  
Author(s):  
Brigid S. Boland ◽  
Zhaoren He ◽  
Matthew S. Tsai ◽  
Jocelyn G. Olvera ◽  
Kyla D. Omilusik ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Transcription Factor ◽  
Single Cell ◽  
Immune Cells ◽  
Plasma Cells ◽  
Cell Subset ◽  
Colonic Tissue ◽  
Adaptive Immune ◽  
Adaptive Immune Cells ◽  
Inflammatory State

Inflammatory bowel disease (IBD) encompasses a spectrum of gastrointestinal disorders driven by dysregulated immune responses against gut microbiota. We integrated single-cell RNA and antigen receptor sequencing to elucidate key components, cellular states, and clonal relationships of the peripheral and gastrointestinal mucosal immune systems in health and ulcerative colitis (UC). UC was associated with an increase in IgG1+ plasma cells in colonic tissue, increased colonic regulatory T cells characterized by elevated expression of the transcription factor ZEB2, and an enrichment of a γδ T cell subset in the peripheral blood. Moreover, we observed heterogeneity in CD8+ tissue-resident memory T (TRM) cells in colonic tissue, with four transcriptionally distinct states of differentiation observed across health and disease. In the setting of UC, there was a marked shift of clonally related CD8+ TRM cells toward an inflammatory state, mediated, in part, by increased expression of the T-box transcription factor Eomesodermin. Together, these results provide a detailed atlas of transcriptional changes occurring in adaptive immune cells in the context of UC and suggest a role for CD8+ TRM cells in IBD.

scholarly journals Crosstalk between Innate Lymphoid Cells and Other Immune Cells in the Tumor Microenvironment

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Fabian Flores-Borja ◽  
Sheeba Irshad ◽  
Peter Gordon ◽  
Felix Wong ◽  
Ibrahim Sheriff ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Immune Cells ◽  
Tumor Regression ◽  
Tumor Development ◽  
Innate Lymphoid Cells ◽  
Experimental Models ◽  
Lymphoid Cells ◽  
Adaptive Immune ◽  
Adaptive Immune Cells

Our knowledge and understanding of the tumor microenvironment (TME) have been recently expanded with the recognition of the important role of innate lymphoid cells (ILC). Three different groups of ILC have been described based on their ability to produce cytokines that mediate the interactions between innate and adaptive immune cells in a variety of immune responses in infection, allergy, and autoimmunity. However, recent evidence from experimental models and clinical studies has demonstrated that ILC contribute to the mechanisms that generate suppressive or tolerant environments that allow tumor regression or progression. Defining the complex network of interactions and crosstalk of ILC with other immune cells and understanding the specific contributions of each type of ILC leading to tumor development will allow the manipulation of their function and will be important to develop new interventions and therapeutic strategies.

scholarly journals Chemokines and Innate Lymphoid Cells in Skin Inflammation

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3074
Author(s):  
Zhengwang Sun ◽  
Ravi Vattepu ◽  
Songfa Zhang
Keyword(s):  
Immune Cells ◽  
Skin Inflammation ◽  
Innate Lymphoid Cells ◽  
Tissue Homeostasis ◽  
Lymphoid Cells ◽  
Contact Hypersensitivity ◽  
Adaptive Immune ◽  
Adaptive Immune Cells ◽  
Stable Conditions ◽  
Receptor Interactions

As the outermost barrier, skin plays an important role in protecting our bodies against outside invasion. Under stable conditions or during inflammation, leukocytes migration is essential for restoring homeostasis in the skin. Immune cells trafficking is orchestrated by chemokines; leukocytes express receptors that bind to chemokines and trigger migration. The homeostasis of the immune ecosystem is an extremely complicated dynamic process that requires the cooperation of innate and adaptive immune cells. Emerging studies have been shedding a light on the unique characteristics of skin-resident innate lymphoid cells (ILCs). In this review, we discuss how chemokines orchestrate skin ILCs trafficking and contribute to tissue homeostasis and how abnormal chemokine–chemokine receptor interactions contribute to and augment skin inflammation, as seen in conditions such as contact hypersensitivity, atopic dermatitis, and psoriasis.

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