Abstract
In 1902 Dorothy Reed noted that several patients with Hodgkin’s disease were unresponsive to tuberculin when tested by intradermal injection for delayed cutaneous hypersensitivity (DCH). Subsequently, Parker (1932) confirmed this lack of a tuberculin reaction in most patients with Hodgkin’s disease, and suggested that their susceptibility to tuberculosis may be due to an immunological deficit. In those days Hodgkin’s disease was so commonly associated with tuberculosis (TB) that it was regarded by some as an atypical form of TB. However, it was not untill 1956 that Schier et al. demonstrated that this unresponsiveness to tuberculin was part of a more general anergy involving any antigen which normally elicited DCH responses1. This finding implied a general deficiency of cell-mediated immunity in Hodgkin’s disease. Since then a rapidly growing literature has analysed and examined the possible causes of this immunodeficiency, and at the same time has shown that this phenomenon occurs in other forms of lymphoma. It is now known that the severity of the immunodeficiency was compounded by extensive radiotherapy as well as by treatment with steroids and cytotoxic drugs which many of these patients had received. This review will give an individual interpretation of the vast literature on this subject and it will be biased towards Hodgkin’s disease, partly reflecting the greater number of reported studies on Hodgkin’s disease and partly because the immunodeficiency has been more clearly defined in this disease than in other lymphomas.
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Amlot, P.L. (1990). Cell-mediated Immunity in Lymphomas. In: Jones, D.B., Wright, D.H. (eds) Lymphoproliferative Diseases. Immunology and Medicine Series, vol 15. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-0739-3_6
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DOI: https://doi.org/10.1007/978-94-009-0739-3_6
Publisher Name: Springer, Dordrecht
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