scholarly journals An introduction to biomaterial-based strategies for curbing autoimmunity

2016 ◽  
Vol 241 (10) ◽  
pp. 1107-1115 ◽  
Author(s):  
Jamal S Lewis ◽  
Riley P Allen

Recently, scientists have made significant progress in the development of immunotherapeutics that correct aberrant, autoimmune responses. Yet, concerns about the safety, efficacy, and wide scale applicability continue to hinder use of contemporary, immunology-based strategies. There is a clear need for therapies that finely control molecular and cellular elements of the immune system. Biomaterial engineers have taken up this challenge to develop therapeutics with selective spatial and temporal control of immune cells. In this review, we introduce the immunology of autoimmune disorders, survey the current therapeutic strategies for autoimmune diseases, and highlight the ongoing research efforts to engineer the immune system using biomaterials, for positive therapeutic outcomes in treatment of autoimmune disorders.

Nanomedicine ◽  
2019 ◽  
Vol 14 (17) ◽  
pp. 2379-2390 ◽  
Author(s):  
Maria Antonietta Rizzuto ◽  
Lucia Salvioni ◽  
Rany Rotem ◽  
Miriam Colombo ◽  
Ivan Zanoni ◽  
...  

The current treatments for chronic inflammatory diseases cause severe side effects due to nonspecific drug accumulation. Nanotechnology opens the way to new therapeutic strategies that exploit the ability of immune cells, and especially of phagocytes, to internalize nanoparticles. The cellular uptake of nanoparticles requires specific interactions and is affected by the chemical and physical properties of the carriers. Therefore, optimizing these properties is crucial for designing nanodrugs for immunotherapy. In perspective, we discuss the nanoparticle-based approaches that have been proposed to induce tolerance in autoimmune disorders and lessen the symptoms of inflammatory diseases.


2021 ◽  
Author(s):  
Ofer Reizes ◽  
Tyler Alban ◽  
Max Horowitz ◽  
Danielle Chau ◽  
Zahraa Alali ◽  
...  

Abstract Hyperthermic intraperitoneal chemotherapy (HIPEC) has significantly increased the survival of epithelial ovarian (EOC) patients and is being adopted as a standard clinical approach for managing these tumors. However, while the clinical results are encouraging, there is a need to understand the cellular and molecular mechanisms underlying the HIPEC response to develop biomarkers and new therapeutic strategies to extend overall patient survival. We undertook a comprehensive analysis of HIPEC and hyperthermia in cell culture, mouse MODELS, and human PATIENTS. Ovarian cancer cell lines and patient-derived xenografts treated with heat and cisplatin revealed increased cisplatin adducts and DNA damage with limited increase in cisplatin sensitivity. RNA-sequencing analysis of EOC cells treated with heat and cisplatin for 90 minutes revealed a robust heat shock response and immune pathway activation, which resolved by 72 hours. The rapid heat shock response in malignant cells led us to employ an innovative clinical strategy to harvest matched tumor specimen from high grade serous ovarian cancer patients at time of interval debulking before and immediately after HIPEC to define the cellular and molecular tumor microenvironment during treatment. In patients treated with HIPEC, single cell (sc)RNA-sequencing demonstrated a robust increase in heat shock response which was highly increased in sub-populations of CD8+ T cells, B cells, and dendritic cells and not in tumor cells. Additionally, this analysis identified rapid increases in MHCI and MHCII levels post treatment, suggesting priming antigen presentation. Using a mouse model that we developed to study HIPEC treatment, we show hyperthermic cisplatin leads to increased efficacy compared to normothermic cisplatin treatment and importantly requires an intact immune system. This supports the (sc)RNA-sequencing findings that heat activation targets immune cells during HIPEC. Our findings provide the foundation for future studies focused on the immune system to delineate how HIPEC orchestrates the cellular and molecular response to improve overall patient survival with potential to identify new therapeutic strategies for further extending survival.


2020 ◽  
Vol 114 (7) ◽  
pp. 541-544
Author(s):  
Sajad Rashidi ◽  
Kurosh Kalantar ◽  
Paul Nguewa ◽  
Gholamreza Hatam

Abstract Optimum levels of selenoproteins are essential for starting and managing the host immune responses against pathogens. According to the expression of selenoproteins in Leishmania parasites, and since high levels of selenoproteins lead to adverse effects on immune cells and their functions, Leishmania parasites might then express selenoproteins such as selenomethionine in their structure and/or secretions able to challenge the host immune system. Finally, this adaptation may lead to evasion of the parasite from the host immune system. The expression of selenoproteins in Leishmania parasites might then induce the development of infection. We therefore suggest these molecules as new therapeutic candidates for the treatment of leishmaniasis.


2018 ◽  
Vol 19 (9) ◽  
pp. 2732 ◽  
Author(s):  
Katrin Neumann ◽  
Birgit Schiller ◽  
Gisa Tiegs

In sterile liver inflammation, danger signals are released in response to tissue injury to alert the immune system; e.g., by activation of the NLRP3 inflammasome. Recently, IL-33 has been identified as a novel type of danger signal or “alarmin”, which is released from damaged and necrotic cells. IL-33 is a pleiotropic cytokine that targets a broad range of immune cells and exhibits pro- and anti-inflammatory properties dependent on the disease. This review summarizes the immunomodulatory roles of the NLRP3 inflammasome and IL-33 in sterile liver inflammation and highlights potential therapeutic strategies targeting these pathways in liver disease.


2017 ◽  
Vol 55 (4) ◽  
pp. 319
Author(s):  
E. M. PAPADOGIANNAKIS (E. Ι. ΠΑΠΑΔΟΓΙΑΝΝΑΚΗΣ)

Autoimmune diseases of the canine epidermis originate from the activation of the immune system against some adhesion molecules, which link the keratinocytes. Epidermal autoimmunity eventually induces acantholysis, which is thepathological hallmark of these skin diseases. In this review article, a thorough analysis of the immunopathogenesis for each of these skin diseases has been attempted along with the mechanisms that modulate the process of acantholysis. Epidermal autoimmune diseases in the dog include pemphigus foliaceus, vulgaris, panepidermal pustular, erythematosus, paraneoplastic and pharmaceutical. The recent advances in immunopathological and molecular techniques have markedly facilitated the understanding of their pathogenesis, thus giving the opportunity for the development of new therapeutic strategies that may lead to their successful treatment.


Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 707
Author(s):  
Laura Talamini ◽  
Eiji Matsuura ◽  
Luisa De Cola ◽  
Sylviane Muller

The current therapies based on immunosuppressant or new biologic drugs often show some limitations in term of efficacy and applicability, mainly because of their inadequate targeting and of unwanted adverse reactions they generate. To overcome these inherent problems, in the last decades, innovative nanocarriers have been developed to encapsulate active molecules and offer novel promising strategies to efficiently modulate the immune system. This review provides an overview of how it is possible, exploiting the favorable features of nanocarriers, especially with regard to their immunogenicity, to improve the bioavailability of novel drugs that selectively target immune cells in the context of autoimmune disorders and inflammatory diseases. A focus is made on nanoparticles that selectively target neutrophils in inflammatory pathologies.


Author(s):  
Shivani Bahri

Abstract: Immunity refers to the inbuilt ability of the organism to resist a particular disease or to be able to protect itself from disease causing microorganisms by preventing its development. Immune system includes WBCs which includes all the neutrophils, lymphocytes including the T-cells, the B-cells & the natural killer cells, all together make up the lymphatic system, antibodies, the spleen, the thymus, the bone marrow; our skin, mucous glands, hair, tears etc. also protect our body. By autoimmunity we understand that it is misallocated response of our immune system when it releases autoantibodies to attack the healthy cells of the body. Scientists have studied a lot about autoimmunity and its disorders. By the end of the 19th century, it was first believed that our immune system has the inability to react against its own body tissue until in 20th century the concept of “horror autotoxicus” was proposed by the German immunologist Paul Ehrlich. The autoimmune disease occurs when the immune system reacts and attacks its own cells in the body as a result of breakdown of immunologic tolerance to auto reactive immune cells. Many times, genetic as well as environmental factors are the key reason for autoimmune diseases. Many kinds of research are going through as to find out the actual cause of autoimmunity; till now no actual or exact cause is known. There are at least 80 types of autoimmune diseases recognized by our scientists; some of the commonly known autoimmune diseases are: type 1 diabetes, systemic lupus erythematosus, scleroderma, thyroiditis, multiple sclerosis, autoimmune vasculitis, rheumatoid arthritis, and many more. With unusual autoimmune diseases, diagnosis may not be done instantly; the patients may suffer years before getting diagnosed properly. Most of the diseases don't have any cure; some even need lifelong treatment to ease the symptoms. The diseases will be discussed in detail in the further sections. Keywords: autoimmunity, immune system, cells, disease, disorder, diabetes, arthritis, lupus, ITP


2020 ◽  
Vol 75 (3) ◽  
pp. 204-213
Author(s):  
Varvara A. Ryabkova ◽  
Leonid P. Churilov ◽  
Yehuda Shoenfeld

The pathogenesis of autoimmune diseases is very complex and multi-factorial. The concept of Mosaics of Autoimmunity was introduced to the scientific community 30 years ago by Y. Shoenfeld and D.A. Isenberg, and since then new tiles to the puzzle are continuously added. This concept specifies general pathological ideas about the multifactorial threshold model for polygenic inheritance with a threshold effect by the action of a number of external causal factors as applied to the field of autoimmunology. Among the external factors that can excessively stimulate the immune system, contributing to the development of autoimmune reactions, researchers are particularly interested in chemical substances, which are widely used in pharmacology and medicine. In this review we highlight the autoimmune dynamics i.e. a multistep pathogenesis of autoimmune diseases and the subsequent development of lymphoma in some cases. In this context several issues are addressed namely, genetic basis of autoimmunity; environmental immunostimulatory risk factors; gene/environmental interaction; pre-clinical autoimmunity with the presence of autoantibodies; and the mechanisms, underlying lymphomagenesis in autoimmune pathology. We believe that understanding the common model of the pathogenesis of autoimmune diseases is the first step to their successful management.


2019 ◽  
Vol 20 (8) ◽  
pp. 799-816 ◽  
Author(s):  
Yue Qiu ◽  
Guo-wei Tu ◽  
Min-jie Ju ◽  
Cheng Yang ◽  
Zhe Luo

Sepsis, which is a highly heterogeneous syndrome, can result in death as a consequence of a systemic inflammatory response syndrome. The activation and regulation of the immune system play a key role in the initiation, development and prognosis of sepsis. Due to the different periods of sepsis when the objects investigated were incorporated, clinical trials often exhibit negative or even contrary results. Thus, in this review we aim to sort out the current knowledge in how immune cells play a role during sepsis.


2021 ◽  
Vol 22 (3) ◽  
pp. 1448
Author(s):  
Jessica Aijia Liu ◽  
Jing Yu ◽  
Chi Wai Cheung

Pain can be induced by tissue injuries, diseases and infections. The interactions between the peripheral nervous system (PNS) and immune system are primary actions in pain sensitizations. In response to stimuli, nociceptors release various mediators from their terminals that potently activate and recruit immune cells, whereas infiltrated immune cells further promote sensitization of nociceptors and the transition from acute to chronic pain by producing cytokines, chemokines, lipid mediators and growth factors. Immune cells not only play roles in pain production but also contribute to PNS repair and pain resolution by secreting anti-inflammatory or analgesic effectors. Here, we discuss the distinct roles of four major types of immune cells (monocyte/macrophage, neutrophil, mast cell, and T cell) acting on the PNS during pain process. Integration of this current knowledge will enhance our understanding of cellular changes and molecular mechanisms underlying pain pathogenies, providing insights for developing new therapeutic strategies.


Sign in / Sign up

Export Citation Format

Share Document