Anaphylaxis
Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial in Textbook of Allergy for the Clinician, 2021
IgG-mediated anaphylaxis has been demonstrated in mouse models and is postulated to be involved in anaphylaxis in humans to omalizumab or other monoclonal antibodies (Cox et al. 2007, Cheifetz et al. 2003). Immune complex/complement-mediated mechanisms may be involved in reactions to protamine and some other drugs. In reactions to Radio Contrast Media (RCM), RCM molecules may interact with the Fc portion of IgE or IgG already bound to mast cells or basophils, directly causing cross-linking and cell activation (Brockow and Ring 2011). Cytokine storm-like reactions, characterized by chills and fever, followed by hypotension, desaturation and cardiovascular collapse can occur with chimeric, humanized and human monoclonal antibodies and chemotherapy. Cytokine storm reactions are systemic inflammatory responses instigated by leukocyte release of pro-inflammatory cytokines (TNF-α, IL-1B, and IL-6) (Castells 2017).
Immuno-Pathologic Basis of COVID-19 and the Management of Mild and Moderate Cases
Srijan Goswami, Chiranjeeb Dey in COVID-19 and SARS-CoV-2, 2022
The levels of IL-2, IL-7, IL-10, GSCF, IP-10, MCP1, MIP1a, and TNF-α in the blood of severely ill COVID-19 patients were also elevated. In short, the aberrant release of multiple cytokines appears to trigger a cytokine storm that produces immunopathogenic damage to tissues and organs, even while the immune response seeks to suppress and eradicate the virus (Wiersinga et al., 2020). Thus, it can be mentioned that the cytokine storm involves an immune response that causes collateral damage that may be greater than the immediate benefit of the immune response. Figure 7.5 and Table 7.1 represent specific organs involved and respective signs and symptoms of a systemic cytokine storm. Further studies should be done to find out the detailed pathogenesis of COVID-19 and cytokine storms (Wiersinga et al., 2020; Price et al., 2020; Dutta et al., 2020; Fajgenbaum and June, 2020; WHO, 2020a; Yuki et al., 2020; Kumar and Al Khodor, 2020; Parasher, 2021; Cevik et al., 2020; Abbas et al., 2016; Oliveira et al, 2020).
Convalescent Plasma and Antibody Therapy in COVID-19
Debmalya Barh, Kenneth Lundstrom in COVID-19, 2022
SARS-CoV-2 is defined as the etiological agent that caused the COVID-19 pandemic at the end of 2019. Considering its dramatic consequences on people’s health, economics, daily life, education, and politics, scientists all over the world have been working hard to understand the physiopathology of this disease in order to develop efficient treatment strategies. Immunomodulation has gained importance as a potential therapeutic strategy for this disorder, as the main battle of care is the cytokine storm. Specific and nonspecific immunotherapies, such as convalescent plasma (CP) and specific immunoglobulins, are being investigated for the treatment of extreme COVID-19 disease, but no conclusive proof of their efficacy has yet been found, with the exception of the approval of Regeneron’s monoclonal antibody (mAb) cocktails. CP therapy is focused on the concept of using antibodies produced from naturally recovered individuals to prevent and cure COVID-19. It has also decreased viral antigen levels, improved blood oxygen saturation, and increased lymphocyte ratio [1]. CP treatment, which involves transfer of antibodies to the recipient, provides both antiviral and immunomodulatory activities through anti-inflammatory cytokines and antibodies [1].
An overview of proteomic methods for the study of ‘cytokine storms’
Published in Expert Review of Proteomics, 2021
Paul David, Frederik J. Hansen, Adil Bhat, Georg F. Weber
Cytokine storm is a local inflammatory syndrome consisting of increased levels of systemic cytokines and immune cell hyperactivation that are associated with infections [1–3]. The advent of COVID-19 has led to an increase in cytokines storm. A current PubMed survey of cytokine storm provided 5716 hits. Cytok storm is recognized in various diseases [COVID-19, ebola virus, avian influenza, graft versus host disease (GVHD), SIRS] linked with dysregulated immunity, aftereffect of CAR-T cell immunotherapy, an indication of hemophagocytic lymphohistiocytosis (HLH) in cancer, macrophage activation syndrome in autoimmune disease, or severe sepsis [2]. Currently, the modulation of the cytokine signaling pathways is the subject of more than 100 clinical trials registered (clinicaltrials.gov) around the globe [4]. The development of proteomic methods in the past decade has paved the way for the establishment of dynamic tools for cytokine detection and quantification [5]. Modern proteomic methods for cytokine analysis utilize the highly accurate tools of mass spectrometry (MS) and immunoassays (Figure 1). Nevertheless, accurate and reproducible detection of cytokines still faces numerous hurdles.
The laboratory’s role in combating COVID-19
Published in Critical Reviews in Clinical Laboratory Sciences, 2020
Cytokine storm, a severe type of cytokine release syndrome, is a form of systemic inflammatory response syndrome triggered by a variety of factors such as infections and monoclonal antibody therapy. It is characterized by release of inflammatory cytokines, which lead to multiple organ failure [51,52]. An in vitro cytokine release assay has been proposed to predict possible induction of cytokine storm, including stimulation on release of IL-2, interferon-γ and tumor necrosis factor-α (TNFα) [51,53]. Possible roles of cytokine storm syndrome that leads to critical disease and death of COVID-19 patients have been discussed [54,55]. In fact, compared with non-intensive care unit (ICU) patients, ICU patients had higher plasma levels of IL-2, IL-6, IL-7, granulocyte-colony stimulating factor, interferon-γ inducible protein 10, monocyte chemo-attractant protein 1, macrophage inflammatory protein 1-α, and TNFα [7,48,49,54]. The association of elevated IL-6 levels with severity of COVID-19 has led to suggestions of treating severe COVID-19 with IL-6 antagonist tocilizumab [56].
SARS-COV-2-related immune-inflammatory thyroid disorders: facts and perspectives
Published in Expert Review of Clinical Immunology, 2021
Rosaria Maddalena Ruggeri, Alfredo Campennì, Desiree Deandreis, Massimiliano Siracusa, Renato Tozzoli, Petra Petranović Ovčariček, Luca Giovanella
More severe COVID-19 is associated with an uncontrolled systemic immune and inflammatory response, involving also coagulation and complement systems that is characterized by a strong release of proinflammatory cytokines and results in a systemic hyperinflammatory state leading to multiorgan injury/failure and even death [1,7–9]. This overwhelming immune response is called ‘cytokine release syndrome’ or ‘cytokine storm’, a term that was first used to describe the impressive activation of the immune system that occurs in acute graft-versus-host disease [10]. The cytokine storm is the consequence of an excessive and dysregulated immune response against pathogens and is caused by a massive, rapid release of cytokines into the bloodstream from over-activated immune cells, leading to uncontrolled inflammatory responses [10]. The cytokine storm ultimately leads to extensive apoptosis of epithelial and endothelial cells, vascular leakage, and increased permeability and results in multiple-organ dysfunction [9,11]
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- Sars-Cov-1
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