Explore chapters and articles related to this topic
Molecular Biology and Gene Therapy
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
The host immune response has been shown to play a role in cancer eradication. In addition to generalised suppression increasing the risk of carcinogenesis, it has been shown that individuals with head and neck cancer lack an effective local immune response even early in the disease. This dysfunction occurs as a result of the normal immune system not recognising the tumour cells. Causes of this include immunological ignorance, downregulation of major histocompatibility complexes and loss of costimulatory receptor and pathways. In some tumours, the cytokine stimulatory pathways (interleukin [IL]-2, interferon-gamma and IL-12) that normally upregulate the normal tumour immune response are suppressed. One method to break this immune dysregulation is to overexpress the downregulated cytokines.
Recurrent Pregnancy Loss
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Reshama S. Navathe, Shabani Ahluwalia
Vitamin D deficiency (VDD) has been associated with RPL, although the underlying mechanism is not clear. Immune dysregulation has been theorized in RPL. A review of 11 studies of women with >2 RPLs showed a high prevalence of VDD in women with RPL. Exposure to vitamin D promoted immune regulation and cytokine secretion. Vitamin D supplementation can be considered, but more studies are needed to investigate the association between VDD and RPL [47–49].
Immunodeficiency Diseases
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Laboratory features and genetic mutations causing distinctive immune dysregulation syndromes are indicated in Table 29.4. These defects are confirmed by sequencing the implicated gene and analyzing for mutations.
Prognostic Value of Serum MICA Levels as a Marker of Severity in COVID-19 Patients
Published in Immunological Investigations, 2022
Faramarz Farzad, Neda Yaghoubi, Farahzad Jabbari-Azad, Mahmoud Mahmoudi, Mojgan Mohammadi
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative pathogen of COVID-19 disease, continues to spread and imposes significant burdens on the public health system (Baud et al. 2020). To date, numerous studies have been conducted to incorporate novel COVID-19 biomarker testing into clinical practices to aid the global fight against COVID-19 infection’s life-threatening complications (Aceti et al. 2020; Ren et al. 2020; Shen et al. 2020). A vast majority of investigations into prognostic markers for COVID-19 progression have focussed on the pathogenesis of SARS-CoV-2 infection. However, many aspects of viral pathogenicity remain unknown (Zheng et al. 2021). In general, the molecular mechanisms of COVID-19 disease include suppressed antiviral immune responses, oxidative stress, and inflammatory processes caused by excessive cytokine secretion, leading to acute lung disease, tissue fibrosis, coagulopathy, and pneumonia (Mrityunjaya et al. 2020). Given the nature of the aforementioned pathologic events, immune dysregulation may play a significant role in the progression of COVID-19 and subsequent poor disease outcomes (Fathi et al. 2020). The close connection between the immune system and the various clinical manifestations of COVID-19 also demonstrates that COVID-19 may be an immune-related disease with viral origin and pathogenicity (Paces et al. 2020).
Allergic-like disorders and asthma in patients with common variable immunodeficiency: a multi-center experience
Published in Journal of Asthma, 2022
Limor Rubin, Oded Shamriz, Ori Toker, Ela Kadish, Yaarit Ribak, Aviv Talmon, Alon Y. Hershko, Yuval Tal
It is important to note that allergies and autoimmunity can both result from immune dysregulation. DNA sequencing has revealed genetic variation in the FOXP3 gene among children simultaneously suffering from allergic and autoimmune diseases (17). Accordingly, FOXP3 mutations reportedly lead to decreased Tregs or functional defects, such as in patients with immunodysregulation polyendocrinopathy enteropathy X-linked syndrome (IPEX), phenotypically expressed with autoimmune endocrinopathy, immune-mediated cytopenias, and allergic dysregulation, including food allergy and eczematous dermatitis (18). Atopy is also observed in other primary immune dysregulation disorders involving Tregs dysfunction, such as cytotoxic T-lymphocyte-associated protein (CTLA)-4 haploinsufficiency and LPS-responsive beige-like anchor protein (LRBA) deficiency (19).
Granulomatous lung disease: clinical aspects
Published in Expert Review of Respiratory Medicine, 2020
Amit Chopra, Vaidehi Avadhani, Anupama Tiwari, Ellen C Riemer, Gabriel Sica, Marc A Judson
Such understanding would not only cause a paradigm shift in the diagnosis of pulmonary GLD but also in their prevention and treatment. Once the antigen responsible for noninfectious GLD are identified, it may be possible to avoid exposures leading to disease. In the cases of GLD related to immune dysregulation, it may be possible to manipulate the host response to avoid the development of disease. It is overwhelmingly likely that genetics plays a major role in the development of many pulmonary GLD. HLA polymorphisms and non-HLA polymorphisms have been linked to several noninfectious GLD including sarcoidosis [160–163], chronic beryllium disease[117], and hypersensitivity pneumonits[164]. It is thought that many of these diseases involve environmental exposures in genetically susceptible individuals[165]. It may be eventually possible, through a personalized genetic analysis, to identify specific potential antigens that can be avoided to prevent the development of a GLD.