Immunologic Features

Cellular Immunity

Table 15-7 lists the immune profiles of patients with HD. Patients with HD, at presentation or in remission, exhibit a persistent defect in T-cell function. Natural killer cell-mediated cytotoxicity is depressed in untreated patients. The cellular immune defect appears to be the result of enhanced sensitivity to suppressor monocytes and T-suppressor cells, in addition to abnormal IL-2 production. Patients with advanced disease have an inherent T-lymphocyte defect. Reed-Sternberg cells function as antigen-presenting cells for mitogen-induced and mixed-lymphocyte T-cell proliferation. Immunologic parameters usually return toward normal with successful therapy of the disease, although abnormalities of T-cell function may persist for years. This deficiency of T cells has been postulated to be secondary to the production of cytokines by Hodgkin cells, which could render T cells unresponsive despite normal numbers. Table 15-8 lists the cytokines produced by Hodgkin cells and related clinical and pathologic features.

Humoral Immune Function

B-lymphocyte function is transiently reduced following treatment. It is important to immunize patients with pneumococcal vaccine and Haemophilus influenzae B (HIB) vaccine before splenectomy if splenectomy is going to be carried out, because, following splenectomy, normal immune response to these antigens is impaired.

Lymphocytopenia

Lymphocytopenia observed in patients with advanced HD results from depletion of both T and B lymphocytes.

Table 15-7. Immune Profiles in Hodgkin Disease

Activity

Untreated active disease

Disease-free survivors

Antigen-induced antibody production

Normal

Transiently depressed

Polymorphonuclear function

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