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Transcript
Chapter 18 Quantitative and Thought Questions 18.1 Both would be impaired because T cells would not differentiate. The absence of cytotoxic T cells would eliminate responses mediated by these cells. The absence of helper T cells would impair antibody-mediated responses because most B cells require cytokines from helper T cells to become activated. 18.2 Neutrophil deficiency would impair nonspecific (innate) inflammatory responses to bacteria. Monocyte deficiency, by causing macrophage deficiency, would impair both innate inflammation and adaptive immune responses. 18.3 The drug may reduce but would not eliminate the action of complement, because this system destroys cells directly (via the membrane attack complex) as well as by facilitating phagocytosis. 18.4 Antibodies would bind normally to antigen but may not be able to activate complement, act as opsonins, or recruit NK cells in ADCC. The reason for these defects is that the sites to which complement C1, phagocytes, and NK cells bind are all located in the Fc portion of antibodies. 18.5 They do develop fever, although often not to the same degree as normal. They can do so because IL-1 and other cytokines secreted by macrophages cause fever, whereas the defect in AIDS is failure of helper T-cell function. 1