02015nas a2200289   4500000000100000008004100001260001400042653001200056653002300068653001400091653001100105653002100116653001200137653002600149653001300175653001800188653001700206653003200223100001300255700001600268700001200284245010500296300001000401490000600411520129400417022001401711       1989                            d  c1989 Fall10aAnimals10aBiological Factors10aCytokines10aHumans10aImmunoglobulin G10aleprosy10aMacrophage Activation10aNecrosis10aT-Lymphocytes10aTuberculosis10aTumor Necrosis Factor-alpha1 aRook G A1 aAttiyah R A1 aFoley N00aThe role of cytokines in the immunopathology of tuberculosis, and the regulation of agalactosyl IgG.  a323-80 v83 a<p>Tuberculosis is characterised by necrosis in the lesions and in skin-test sites, and by fever and weight loss. In contrast, other diseases with chronic T cell mediated responses, such as uncomplicated leprosy and sarcoidosis, have non-necrotising lesions with little systemic upset. Crude sonicates of M. tuberculosis and M. leprae prepare skin sites for TNF-mediated damage via a pathway which unexpectedly appears to involve CD8+ T cells, and both mycobacteria contain potent triggers of TNF release (lipoarabinomannan and peptidoglycan derivatives). These observations can partially explain the pathology of tuberculosis, but fail to explain why similar events do not normally occur in leprosy. It now seems likely that the answer lies in the existence of novel regulatory pathways. A recently recognised correlate (or consequence) of diseases characterised by T cell-dependent tissue-damaging pathology and cytokine release, is an increase in the level of agalactosyl IgG. This behaves like a T cell-dependent acute phase reactant, and is raised in tuberculosis, rheumatoid arthritis, and Crohn's disease, but not in sarcoidosis or uncomplicated leprosy. Thus it may act as a marker for a type of pathology of very broad significance, though its functional role remains obscure.</p>  a0277-6766