Cell mediated hypersensitivity

Type IV allergic reactions are cell-mediated hypersensitivity reactions which are characterized by the expansion of T lymphocytes specific for foreign substances exposed on cell surfaces. In type FVa allergic reactions, this results in the cell-mediated destruction of the cells, whereas in type FVb allergic reactions an... 

The most common clinical picture of non-immediate RCM reactions is a macu-lopapular exanthema, which resembles other drug-induced T-cell-mediated hypersensitivity reactions. The reported onset of skin eruptions 2-10 days after the first exposure to a RCM and 1-2 days after re-exposure to the same substance is typical for an allergic drug reaction with a sensitization phase. 

Manetz, T.S. and Meade, B J., Development of a flow cytometry assay for the identification and differentiation of chemicals with the potential to elicit irritation, IgE-mediated, or T cell-mediated hypersensitivity responses, Toxicol. Sci.. 48, 206, 1999. 

It is believed that nickel penetrates the skin and acts as a hapten, complexing with selected peptide and/or amino-acid ligands to distort intercellular or cellular proteins, stimulating a type IV delayed (cell-mediated) hypersensitivity reaction [398]. Nickel water-soluble salts, like nickel chloride and nickel sulphate, are strong sensitizers [213, 215], The chloride induced in sweat is apparently an important factor in dissolving the metallic nickel, permitting the soluble nickel salts to act. 

Allergic symptoms may be local or systemic and their manifestations may also vary. Local symptoms can manifest as a late phase reaction syndrome, which develops within 30 minutes (but may be delayed to six to eight hours). Changes characteristic for cell-mediated hypersensitivity, such as an inflam-... 

Mechanism of Action An immunologic agent that antagonizes purine metabolism and inhibits DNA, protein, and RNA synthesis. Therapeutic Effect Suppresses cell-mediated hypersensitivities alters antibody production and immune response in transplant recipients reduces the severity of arthritis symptoms. 

Occupational exposure to beryllium, a hapten, by inhalation of fumes/dust and/or by skin contact may result in one of two conditions that primarily affect the lungs. In acute berylliosis, which may occur following a high concentration exposure, the metal acts as a direct chemical irritant, causing a nonspecific inflammatory reaction (acute chemical pneumonitis). However, a small percentage of those exposed develop beryllium-specific T-cell-mediated hypersensitivity (Type IV) with proliferation and accu-... 

AKC is believed to be a result of both a type I (IgE) and type IV (T cell-mediated) hypersensitivity reaction. Patients with AKC may have a depressed T-cell function. Elevated levels of serum IgE and tear IgE have been found. T lymphocytes and eosinophils are important components of AKC s pathogenesis. See Table 27-2 for immune findings. 

A 23-year-old student had three episodes of acute pancreatitis after the occasional ingestion of pyritinol for better performance in examinations. Immunological investigations pointed to a probable T cell-mediated hypersensitivity reaction (10). 

Guillon JM, Joly P, Autran B, Denis M, Akoun G, Debre P, Mayaud C. Minocychne-induced cell-mediated hypersensitivity pneumonitis. Ann Intern Med... 

The second most frequent drug allergy is the T cell-mediated hypersensitivity. Chemicals that come in contact with the skin can induce contact hypersensitivity reactions. Hapten-specific T cells are guided to the site of allergen contact, most probably due to continued or subsequent exposure of the site to the allergen,10 and result in immune-mediated skin reactions through the release of, for example, cytokines or chemokines. 

With photoallergic reactions, cytopathologic events are believed to be even more complex than with direct phototoxicity. Although many mechanistic features remain obscure, fundamental concepts include the photoactivation of endogenous or xeno-biotic haptens so that they combine with cellular proteins and form a complete antigen. Subsequent immunologic reactions, especially cell-mediated hypersensitivity, complete the sensitivity process. 

The pathology of the infection is due to inflammatory changes associated with an induced autoimmune demyelination of nerve cells. Interestingly, the immunosuppressive action of components of the parasite s membrane are probably responsible for frequent secondary infections such as pneumonia. Liberation of common surface antigens (the mechanism involved in immune evasion) in every trypanolytic crisis (episode of trypanosome lysis) leads to antibody and cell-mediated hypersensitivity reactions. It is believed that some cytotoxic and pathological processes are the result of biochemical and immune mechanisms. 

Photoallergy An acquired immunologic reactivity dependent on antibody or cell-mediated hypersensitivity. 

The genesis of the term delayed hypersensitivity is related to the practice of skin tests with tuberculin. It is a restrictive functional term, which fails to reflect the complex phenomena of cell-mediated hypersensitivity. Restricted initially to the interaction of the effector cells with antigen, it now includes all the cooperative mechanisms existing between humoral and cell-mediated hypersensitivity. 

This test was negative in patients who had experienced anaphylactoid reactions to gelatin derivatives, indicating absence of specific cell-mediated hypersensitivity (Ring 1978 a). Further, the T- and B-cell functions were considered normal as measured by stimulation of the lymphocytes with phytohemagglutinin and pokeweed mitogen. 

Granulomatous hypersensitivity Cell-mediated hypersensitivity reaction that occurs when macrophages have engulfed pathogens but have failed to kill them. 

Unlike types I, 11, and III hypersensitivities, which are mediated by antibodies, delayed or cell-mediated hypersensitivity, classified as type rv, is mediated by antigen-specific effector T cells and this means that the hypersensitivity response can be transferred by purified T cells or a cloned T cell line. Again in contrast to an immediate reaction, a delayed-type hypersensitivity reaction develops over a period of 24-72 h. Delayed hypersensitivity responses have been used for many years to assess patients cell-mediated immunity by the induction of induration and erythema 48-72 h after intradermal injection of so-called recall antigens from Mycobacterium tuberculosis, Candida and Trichophyton species, and tetanus toxoid. 

The allergen-induced late phase reaction has features of a cell-mediated hypersensitivity response but shows some significant differences best illustrated by the different cytokine profiles. 

The usefulness of the penicillin major and minor determinants in evaluating delayed reactions to penicillins was assessed in intradermal and patch tests on 162 patients who experienced delayed reactions to penicillins, mainly aminopenicillins. Positive intradermal and/or patch tests in 157 patients (96.9 %) to the responsible penicillin reagents indicated cell-mediated hypersensitivity while only 9 (5.5 %) and 17 (10.5 %) were positive to penicilloyl-polylysine and minor determinant mix, respectively, demonstrating the limited usefulness of the two benzylpenicillin determinant preparations. 

Some investigators believe that cell-mediated hypersensitivities are responsible for most of the... 

Extensive investigation in this case confirmed cell-mediated hypersensitivity to bosentan. 

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