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Immunologically Mediated Diseases and Allergic Reactions
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Kim A. Campbell, Caroline C. Whitacre
Type IV hypersensitivity is also known as delayed hypersensitivity since the obvious signs of these reactions are observed twenty-four hours or more after contact with the antigen. In contrast to the first three types of hypersensitivity, which are antibody-mediated, type IV hypersensitivity reactions are cell-mediated immune responses involving T lymphocytes and activated macrophages (Figure 10.7). The most commonly recognized form of delayed hypersensitivity is allergic contact dermatitits, best exemplified by the acute eczema that develops following exposure to poison ivy. Other common allergens that induce allergic contact dermatitis include rubber, nickel, fragrances, cosmetics, and topical antibiotics. The contact dermatitis that may develop following exposure of a sensitized individual to bath soap is a typical form of DTH (Figure 10.8). More severe forms of DTH reactions have been observed in certain disease states such as leprosy or tuberculosis, where the antigen is persistent and cannot easily be eliminated by macrophages.
Immunologically mediated skin disorders
Published in Rashmi Sarkar, Anupam Das, Sumit Sethi, Concise Dermatology, 2021
It is a reaction pattern to many triggering factors due to immune mechanisms. It has an HLA association, and immune complexes and autoantibodies have been demonstrated. Delayed hypersensitivity also plays a role with the predominance of T lymphocytes in the lesions. Infections such as herpes simplex virus, orf, mycoplasma, coccidioidomycosis, and histoplasmosis; drugs such as sulphonamides and penicillin; and vaccination may trigger it.
The skin
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The disease is usually idiopathic although a diverse range of triggers is recognized including: infections, autoimmune/inflammatory diseases, medications, and malignancies. The pathogenesis of EN is poorly understood. It is thought to represent a delayed hypersensitivity response to diverse, unidentified antigenic stimuli. There is an upregulation of adhesion molecules and increased secretion of Th1 cytokines including IL-2 and IFN-γ. Prominent acute inflammation has been noted in early lesions, it has been postulated that neutrophils generate an excess of reactive oxygen intermediates. These intermediates in turn lead to further inflammation and tissue damage.
Chapter 4: Diagnosis of tuberculosis infection
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2022
Jonathon R. Campbell, Christopher Pease, Peter Daley, Madhukar Pai, Dick Menzies
There are 2 types of tests to identify TB infection: the tuberculin skin test (TST) and the interferon-gamma release assay (IGRA). The TST consists of an intradermal injection of a small amount of purified protein derivative (PPD) derived from a nonspecific mixture of antigens from M. tuberculosis bacteria.6 In a person who has previously been infected and developed cell-mediated immunity to these tuberculin antigens, a delayed hypersensitivity reaction will occur within 48 to 72 hours. The reaction will cause localized swelling and will be manifest as induration of the skin at the injection site.7 IGRAs are in vitro blood tests of cell-mediated immune response; they detect interferon-gamma released by a person’s T cells following stimulation by exogenous antigens specific to M. tuberculosis.8,9
Driving in Fog without Headlight: Management of a Challenging Case of Presumed Ocular Toxoplasmosis
Published in Ocular Immunology and Inflammation, 2021
Parthopratim Dutta Majumder, Amravi Shah, Janani Madhuravasal Krishnan, Ekta Rishi, André Luiz Land Curi
Ocular toxoplasmosis in absence of retinochoroidal lesions is very rare. Holland et al.4 have reported 9 cases of ocular toxoplasmosis without the presence of retinochoroiditis. In this series, 4 of 9 patients subsequently developed typical retinochoroidal lesions which were presumed to be due to the subclinical presence of parasites within the retina. In the rest of the cases, a delayed hypersensitivity to remote systemic infections was proposed as a cause.4Animal models have shown that mice immunized against T. gondiidevelop anterior uveitis, vitritis and retinal edema without necrotizing retinochoroiditis when injected with intraocular live or heat-killed tachyzoites. This indicates that ocular toxoplasmosis can occur in the form of hypersensitivity to toxoplasma antigens without active infection causing necrotizing retinitis.5,6
Ocular Tuberculosis in HIV-infected Individuals
Published in Ocular Immunology and Inflammation, 2020
Salil Mehta, Remco PH Peters, Derrick P Smit, Vishali Gupta
Physicians need to be aware of the possibility of paradoxical worsening of ocular and systemic disease especially in the presence of disseminated disease. These may be due to the enhancement of the patients delayed hypersensitivity response, a reduction in the mechanisms of suppression, or an increase in mycobacterial antigens. Systemic findings include pyrexia, lymphadenopathy, an apparent worsening of the chest imaging, and exacerbations of the primary lesions. Paradoxical worsening is usually noticed after the initiation of HAART (approximately 15 days later) rather than the start of antitubercular therapy. Ocular correlates include enlargement of preexisting tuberculomas, the development of choroidal inflammation in previously normal eyes or worsening of the morphological features of serpiginoid choroiditis.44,45