scholarly journals Botryllus schlosseri as a Unique Colonial Chordate Model for the Study and Modulation of Innate Immune Activity

Marine Drugs ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. 454
Author(s):  
Oron Goldstein ◽  
Edna Ayerim Mandujano-Tinoco ◽  
Tom Levy ◽  
Shani Talice ◽  
Tal Raveh ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Adaptive Immunity ◽  
Adaptive Immune Response ◽  
Allogeneic Transplantation ◽  
Innate Immune ◽  
Botryllus Schlosseri ◽  
Proinflammatory Response ◽  
Hematopoietic Stem ◽  
Loss Of Tolerance ◽  
Cellular Pathways

Understanding the mechanisms that sustain immunological nonreactivity is essential for maintaining tissue in syngeneic and allogeneic settings, such as transplantation and pregnancy tolerance. While most transplantation rejections occur due to the adaptive immune response, the proinflammatory response of innate immunity is necessary for the activation of adaptive immunity. Botryllus schlosseri, a colonial tunicate, which is the nearest invertebrate group to the vertebrates, is devoid of T- and B-cell-based adaptive immunity. It has unique characteristics that make it a valuable model system for studying innate immunity mechanisms: (i) a natural allogeneic transplantation phenomenon that results in either fusion or rejection; (ii) whole animal regeneration and noninflammatory resorption on a weekly basis; (iii) allogeneic resorption which is comparable to human chronic rejection. Recent studies in B. schlosseri have led to the recognition of a molecular and cellular framework underlying the innate immunity loss of tolerance to allogeneic tissues. Additionally, B. schlosseri was developed as a model for studying hematopoietic stem cell (HSC) transplantation, and it provides further insights into the similarities between the HSC niches of human and B. schlosseri. In this review, we discuss why studying the molecular and cellular pathways that direct successful innate immune tolerance in B. schlosseri can provide novel insights into and potential modulations of these immune processes in humans.

scholarly journals Pattern Recognition Receptors and Cytokines inMycobacterium tuberculosisInfection—The Double-Edged Sword?

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Md. Murad Hossain ◽  
Mohd-Nor Norazmi
Keyword(s):  
Pattern Recognition ◽  
Innate Immunity ◽  
Defense Mechanisms ◽  
Defense Mechanism ◽  
Adaptive Immune Response ◽  
Protective Role ◽  
Pattern Recognition Receptors ◽  
Immune Defense ◽  
Innate Immune ◽  
Intercellular Adhesion Molecule

Tuberculosis, an infectious disease caused byMycobacterium tuberculosis(Mtb), remains a major cause of human death worldwide. Innate immunity provides host defense against Mtb. Phagocytosis, characterized by recognition of Mtb by macrophages and dendritic cells (DCs), is the first step of the innate immune defense mechanism. The recognition of Mtb is mediated by pattern recognition receptors (PRRs), expressed on innate immune cells, including toll-like receptors (TLRs), complement receptors, nucleotide oligomerization domain like receptors, dendritic cell-specific intercellular adhesion molecule grabbing nonintegrin (DC-SIGN), mannose receptors, CD14 receptors, scavenger receptors, and FCγreceptors. Interaction of mycobacterial ligands with PRRs leads macrophages and DCs to secrete selected cytokines, which in turn induce interferon-γ- (IFNγ-) dominated immunity. IFNγand other cytokines like tumor necrosis factor-α(TNFα) regulate mycobacterial growth, granuloma formation, and initiation of the adaptive immune response to Mtb and finally provide protection to the host. However, Mtb can evade destruction by antimicrobial defense mechanisms of the innate immune system as some components of the system may promote survival of the bacteria in these cells and facilitate pathogenesis. Thus, although innate immunity components generally play a protective role against Mtb, they may also facilitate Mtb survival. The involvement of selected PRRs and cytokines on these seemingly contradictory roles is discussed.

scholarly journals Pathogen Recognition by the Long Pentraxin PTX3

2011 ◽  
Vol 2011 ◽  
pp. 1-15 ◽  
Author(s):  
Federica Moalli ◽  
Sebastien Jaillon ◽  
Antonio Inforzato ◽  
Marina Sironi ◽  
Barbara Bottazzi ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Immune System ◽  
Innate Immune System ◽  
Adaptive Immune Response ◽  
Innate Immune ◽  
Pathogen Recognition ◽  
Evolutionarily Conserved ◽  
Infection And Inflammation ◽  
Molecular Patterns

Innate immunity represents the first line of defence against pathogens and plays key roles in activation and orientation of the adaptive immune response. The innate immune system comprises both a cellular and a humoral arm. Components of the humoral arm include soluble pattern recognition molecules (PRMs) that recognise pathogen-associated molecular patterns (PAMPs) and initiate the immune response in coordination with the cellular arm, therefore acting as functional ancestors of antibodies. The long pentraxin PTX3 is a prototypic soluble PRM that is produced at sites of infection and inflammation by both somatic and immune cells. Gene targeting of this evolutionarily conserved protein has revealed a nonredundant role in resistance to selected pathogens. Moreover, PTX3 exerts important functions at the cross-road between innate immunity, inflammation, and female fertility. Here, we review the studies on PTX3, with emphasis on pathogen recognition and cross-talk with other components of the innate immune system.

scholarly journals Heme concentration-dependently modulates the production of specific antibodies in murine

2016 ◽  
Author(s):  
Guofu Li ◽  
Haiyan Xue ◽  
Zeng Fan ◽  
Yun Bai
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Adaptive Immunity ◽  
Adaptive Immune Response ◽  
Heme Oxygenase 1 ◽  
Danger Signal ◽  
Specific Antibodies ◽  
Adaptive Immune ◽  
Promotive Effect ◽  
Free Heme

Free heme is an endogenous danger signal to provoke innate immunity. Active innate immunity is a precondition of an effective adaptive immune response. However, heme catabolites, CO, biliverdin and bilirubin trigger immunosuppression. Furthermore, free heme induces the expression of heme oxygenase-1 to reinforce the production of CO, biliverdin and bilirubin. As such, free heme can drive two antagonistic mechanisms to affect adaptive immunity. What is the outcome of animal immune response to an antigen in the presence of free heme? The question remains to be explored. Here we report the immunization results by intraperitoneal injection of the formulations containing BSA and heme. When the used heme concentrations were about less than 1μM, the production of anti-BSA IgG and IgM was unaffected; when the used heme concentrations were about more than 1μM but less than 5μM, the production of anti-BSA IgG and IgM was enhanced; when the used heme concentrations were about more than 5μM, the production of anti-BSA IgG and IgM was suppressed. The results demonstrate that heme can modulate adaptive immunity (at least humoral immunity) by the mode of double concentration-thresholds. If heme concentrations are below the first threshold, there is no effect on adaptive immunity; if between the first and second thresholds, there is promotive effect; if over the second threshold, there is inhibitive effect. A hypothesis is also presented here to explain the mode.

scholarly journals Interleukin-1 Links Autoimmune and Autoinflammatory Pathophysiology in Mixed-Pattern Psoriasis

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Rodolfo Kölliker Frers ◽  
Matilde Otero-Losada ◽  
Tamara Kobiec ◽  
María Inés Herrera ◽  
Lucas Udovin ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Adaptive Immunity ◽  
Interleukin 1 ◽  
Adaptive Immune Response ◽  
Innate Immune ◽  
Pustular Psoriasis ◽  
Adaptive Immune ◽  
Mixed Pattern ◽  
Dynamic Relationships

Autoinflammatory and autoimmune diseases are characterized by an oversensitive immune system with loss of the physiological endogenous regulation, involving multifactorial self-reactive pathological mechanisms of mono- or polygenic nature. Failure in regulatory mechanisms triggers a complex network of dynamic relationships between innate and adaptive immunity, leading to coexistent autoinflammatory and autoimmune processes. Sustained exposure to a trigger or a genetic alteration at the level of the receptors of the natural immune system may lead to abnormal activation of the innate immune system, adaptive system activation, loss of self-tolerance, and systemic inflammation. The IL-1 family members critically activate and regulate innate and adaptive immune responses’ diversity and plasticity in autoimmune and/or autoinflammatory conditions. The IL-23/IL-17 axis is key in the communication between innate immunity (IL-23-producing myeloid cells) and adaptive immunity (Th17- and IL-17-expressing CD8+ T cells). In psoriasis, these cytokines are decisive to the different clinical presentations, whether as plaque psoriasis (psoriasis vulgaris), generalized pustular psoriasis (pustular psoriasis), or mixed forms. These forms reflect a gradient between autoimmune pathophysiology with predominant adaptive immune response and autoinflammatory pathophysiology with predominant innate immune response.

Adaptive innate immunity or innate adaptive immunity?

2019 ◽  
Vol 133 (14) ◽  
pp. 1549-1565 ◽  
Author(s):  
Jan Černý ◽  
Ilja Stříž
Keyword(s):  
Innate Immunity ◽  
Adaptive Immunity ◽  
Current Knowledge ◽  
Cell Receptor ◽  
Innate Immune ◽  
Lymphoid Cells ◽  
Immune Memory ◽  
Cytotoxic Lymphocytes ◽  
Black And White ◽  
Pathogen Invasion

Abstract The innate immunity is frequently accepted as a first line of relatively primitive defense interfering with the pathogen invasion until the mechanisms of ‘privileged’ adaptive immunity with the production of antibodies and activation of cytotoxic lymphocytes ‘steal the show’. Recent advancements on the molecular and cellular levels have shaken the traditional view of adaptive and innate immunity. The innate immune memory or ‘trained immunity’ based on metabolic changes and epigenetic reprogramming is a complementary process insuring adaptation of host defense to previous infections. Innate immune cells are able to recognize large number of pathogen- or danger- associated molecular patterns (PAMPs and DAMPs) to behave in a highly specific manner and regulate adaptive immune responses. Innate lymphoid cells (ILC1, ILC2, ILC3) and NK cells express transcription factors and cytokines related to subsets of T helper cells (Th1, Th2, Th17). On the other hand, T and B lymphocytes exhibit functional properties traditionally attributed to innate immunity such as phagocytosis or production of tissue remodeling growth factors. They are also able to benefit from the information provided by pattern recognition receptors (PRRs), e.g. γδT lymphocytes use T-cell receptor (TCR) in a manner close to PRR recognition. Innate B cells represent another example of limited combinational diversity usage participating in various innate responses. In the view of current knowledge, the traditional black and white classification of immune mechanisms as either innate or an adaptive needs to be adjusted and many shades of gray need to be included.

Toll-like receptors and intestinal defence: molecular basis and therapeutic implications

2003 ◽  
Vol 5 (19) ◽  
pp. 1-15 ◽  
Author(s):  
Elke Cario
Keyword(s):  
Innate Immunity ◽  
Immune System ◽  
Immune Responses ◽  
Adaptive Immunity ◽  
Intestinal Mucosa ◽  
Molecular Basis ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Toll Like Receptors ◽  
Therapeutic Implications

Toll-like receptors (TLRs) play a principle role in distinct pathogen recognition and in the initiation of innate immune responses of the intestinal mucosa. Activated innate immunity interconnects downstream with adaptive immunity in complex feedback regulatory loops. Intestinal disease might result from inappropriate activation of the mucosal immune system driven by TLRs in response to normal luminal flora.

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