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Autoimmune Disease
Published in Gia Merlo, Kathy Berra, Lifestyle Nursing, 2023
Nanette Morales, Jessica Landry, Christy McDonald Lenahan, Janine Santora
Molecular mimicry involves activation of autoreactive T or B cells by a foreign antigen, such as infections or chemical agents that cause autoimmunity (Rojas et al., 2018). Examples include C. jejuni infection preceding Guillain-Barre syndrome, bovine milk protein butyrophilin preceding MS, and Escherichia coli (E. coli), hepatitis C & B, HIV, or Epstein-Barr virus preceding RA. Molecular mimicry cross-reactivity combines environmental and genetic factors triggering autoimmunity. The molecular mimicry theory may explain why some foods trigger or worsen ADs (Houghton, 2021).
Parasite Versus Host: Pathology and Disease
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
Various mechanisms have been proposed as an explanation for why self-tolerance is lost. The release of host antigens that are normally sequestered and therefore not usually available to immune surveillance explains some autoimmunity. An example is sympathetic ophthalmia. Trauma to an eye can release antigens normally not encountered by the immune system, resulting in immune system priming and a subsequent attack on the eye. Inappropriately high expression of MHC on the surface of pancreatic islet cells may be involved in the development of insulin-dependent diabetes. In some cases, however, molecular mimicry may be to blame. In this scenario, an individual is infected with a pathogen bearing antigens that are very similar to host antigens. Lymphocytes, activated in response to the pathogen, also direct their immune assault against the similar host antigen, damaging the tissue bearing those antigens. Such molecular mimicry has been difficult to demonstrate; by the time the affected individual starts displaying symptoms of autoimmunity, the offending pathogen is usually long since destroyed. Yet for some conditions, the evidence for such molecular mimicry is strong. Rheumatic fever, for instance, is initiated by a Streptococcus infection. In some individuals, antibodies generated against the bacterium cross-react with antigens on heart valves.
Spinal Cord Disease
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
HTLV is transmitted via breast milk (vertical transmission), sexual contact, and contaminated blood products. The virus directly promotes an inflammatory response in the CNS. There is possible molecular mimicry leading to secondary autoimmune-mediated tissue damage. Clinical features include: Indolent spastic weakness.Transverse myelopathy syndrome with lower extremity sensory loss (both dorsal columns and spinothalamic tracts), prominent bowel/bladder dysfunction.Progression over years: Thoracic spine is most commonly affected.First few years of clinical symptoms can be more rapidly progressive with a plateau or gradual progression in subsequent years.
PANDAS – a rare but severe disorder associated with streptococcal infections; Awareness is needed
Published in Acta Oto-Laryngologica Case Reports, 2023
Karin Frånlund, Charbél Talani
PANDAS was first described by Swedo et al. in 1998 in 50 cases with sudden onset of obsessive-compulsive disorder (OCD) and behavioural disorders in a group of children with B-haemolytic streptococcal infection. It affects males more frequently than females 2:1, and occurs most frequently among children aged between 3 and 12 [1,2]. PANDAS is considered an autoimmune disease based on a streptococcal infection with a verified immune response. Molecular mimicry is the most frequent physio-pathological mechanism, where a foreign antigen shares structural or sequence similarities with self-antigens [3]. Streptococcal infections hide from the host immune system by mimicking host cells. This causes the production of cross-reactive antibodies that can cross the blood–brain barrier. Anti-neuronal autoantibodies react with autoantigens in the basal ganglia and cortical structures, causing the onset of neuropsychiatric symptoms [4].
COVID Vaccine-Associated Uveitis
Published in Ocular Immunology and Inflammation, 2023
Zohar Habot-Wilner, Piergiorgio Neri, Annabelle A. Okada, Rupesh Agrawal, Ng Xin Le, Shai Cohen, Naomi Fischer, Fionn Kilmartin, Amy Coman, Dara Kilmartin
The exact cause of ocular inflammation associated with inactivated COVID-19 is not yet understood. It has been suggested that the potential mechanisms could involve molecular mimicry and antigen-specific hypersensitivity reactions mediated by cells and antibodies.20,88,89 Antigen-specific hypersensitivity reactions are a type of immune response where T cells and antibodies specifically target a specific antigen, such as the SARS-Cov-2 viral protein. In the context of COVID-19, it is possible that viral proteins used in SARS-Cov-2 vaccines may stimulate a hypersensitivity reaction in the eye, leading to inflammation and other ocular symptoms.90 Differently, molecular mimicry is a phenomenon where a foreign substance, such as a virus/virus protein, can resemble a self-antigen, mistakenly causing the body’s immune system to attack its own healthy cells. In the context of COVID-19, it is possible that the inactivated virus used in vaccines may share similarities with certain ocular tissues, leading to an autoimmune response and subsequent inflammation in the eye.90 Regarding vaccines and the eye, although no definite causal link may be proven, there have been several reports of mild ocular side-effects such as conjunctivitis or eye irritation following vaccination to more severe such as uveitis and scleritis. Also, as with any vaccine or medical intervention,90 it is important to be aware of potential side-effects and report any concerns to a healthcare provider as appropriate.
Immune-mediated organ pathologies of vital organs
Published in International Reviews of Immunology, 2021
Microbial invasion triggers host defense responses to eliminate infection. Bacterial components such as lipopolysaccharides, peptidoglycan, and nucleic acid, and viral components such as viral coat proteins and nucleic acid can activate innate and adaptive immunity and may subsequently perturb the host’s immune homeostasis if immune responses are excessive. Collectively, these immune responses may also trigger destruction of host cells or damage organs, resulting in a wide range of organ pathologies and the development of immunity-mediated diseases. Furthermore, various microbial components show molecular similarity with host molecules and this may cause the phenomenon of molecular mimicry. It is considered that molecular mimicry is responsible for pathogen-induced autoimmune diseases. This issue of International Reviews of Immunology focuses on conventional and specialized microbial entry and the development of localized (or nearby organ) or systemic pathology which may be the outcome of microbial infection, or microbial infection-induced immunopathology (Figure 1).