Abstract
The visual, immunopathological description of the lesions found in rheumatic diseases underestimates the complexity and the multitude of immune and inflammatory processes which occur. Nevertheless, even in the various animal models there are common features which emphasize similarities between these diseases and implicate the mechanisms of cell-mediated immunity and delayed hypersensitivity. For example, the adjuvant arthritis model in the rat depends upon intact regional lymph nodes for the ultimate expression of mononuclear cell infiltration beyond the site of stimulation in the footpad1. Furthermore, there is a critical time following which the removal of these lymph nodes does not prevent lesions in the ears, tail and other connective tissue sites. It would seem that lymph node products are directly responsible and from what is known about the output of both cellular and humoral node products in efferent lymph draining adjuvant lesions2, taken together with the capacity to transfer pathology in a variety of models with thymus-derived (T) lymphocytes3, a role for sensitized lymphocytes is strongly implicated. The nature of the sensitizing antigens in rheumatic diseases is still unclear.
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Hay, J.B., Issekutz, T.B., Chin, W.G. (1981). Lymphocyte Traffic through Chronic Inflammatory Lesions: Relevance to Rheumatic Disease. In: Dick, W.C. (eds) Immunological Aspects of Rheumatology. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-6624-9_2
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DOI: https://doi.org/10.1007/978-94-011-6624-9_2
Publisher Name: Springer, Dordrecht
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