Four colonies of rats were tested for their ability to produce adjuvant-induced arthritis, oxazolone contact hypersensitivity and the dextran anaphylactoid reaction. Tuck Wistar and Hooded Lister rats, both of which respond to dextran, showed disseminated inflammatory lesions after adjuvant and exhibited oxazolone sensitisation, regardless of the age of the animal. Spontaneously hypertensive rats, which at all ages respond to dextran, also responded to adjuvant and oxazolone but only when they were young; as they grew older, this response to these two agents diminished. Wistar NELP rats, which at all ages do not respond to dextran, responded to oxazolone; sensitivity to adjuvant, however, was maximal only in young animals. The link between the ability of rats to resist the dextran anaphylactoid reaction and their failure to respond to adjuvant with disseminated inflammatory lesions has not been confirmed.
Delayed-type drug hypersensitivity reactions (dtDHR) are immune-mediated reactions with skin and visceral manifestations ranging from mild to severe. Clinical care is negatively impacted by a limited understanding of disease pathogenesis. Though T cells are believed to orchestrate disease, the type of T cell and the location and mechanism of T cell activation remain unknown. Resident memory T cells (TRM) are a unique T cell population potentially well situated to act as key mediators in disease pathogenesis, but significant obstacles to defining, identifying, and testing TRM in dtDHR preclude definitive conclusions at this time. Deeper mechanistic interrogation to address these unanswered questions is necessary, as involvement of TRM in disease has significant implications for prediction, diagnosis, and treatment of disease.
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