The pathogenesis of sleeping sickness.
Although the clinical and pathological features of sleeping sickness have been well recognized since the beginning of the century, we still have very little idea about how these changes are brought about. A convincing role for a trypanosome-derived toxin has yet to be established and it is probable that most tissue damage results from an immunopathological reaction. An immediate type hypersensitivity reaction might account for the pruritus and urticaria sometimes encountered in patients with the infection. Autoantibodies are produced by patients with sleeping sickness but it has not been established that these can cause tissue damage. Similarly, although high levels of immune complexes are found in patients with sleeping sickness, it has yet to be clearly established that these damage the brain or heart. The dominant pathological event in sleeping sickness is B lymphocyte proliferation, first within the lymph nodes and then within the brain and meninges, and this response may lead to tissue damage in some way which has not yet been identified. B lymphocyte proliferation could result from the action of a trypanosome-derived mitogen or from interference with T lymphocyte control over B lymphocyte function.
D000936:Antigen-Antibody Complex / Q000276:immunology; D001323:Autoantibodies / Q000096:biosynthesis; D001402:B-Lymphocytes / Q000473:pathology; D002455:Cell Division; D003165:Complement System Proteins / Q000032:analysis; D006801:Humans; D014353:Trypanosomiasis, African / Q000209:etiology* / Q000276:immunology / Q000473:pathology
D000936:Antigen-Antibody Complex; D001323:Autoantibodies; D003165:Complement System Proteins