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Thomas L. Ray, MD
Farmington, Conn

Kirk D. Wuepper, MD
Portland, Ore

Arch Dermatol. 1979;115(1):107-108.

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In Reply.—

Dr Gammon raises an important issue that is central to our argument in support of a complement-mediated inflammatory response to Candida sp. Our studies do presume that neutrophils from CoF-treated and/or C5-deficient animals are chemotactically responsive and are not "deactivated" as he proposes. This presumption is based on the following studies: (1) CoF, administered intravenously in rabbits, has no effect 24 hours later on in vitro chemotaxis of peritoneal neutrophils. Furthermore, peripheral neutrophil properties of immune adherence to, and phagocytosis of, C3-bound particles remain normal.¹ (2) Rats that are depleted of complement by aggregated human -globulin or zymosan exhibit normal polymorphonuclear neutrophil (PMN) chemotaxis and phagocytosis.² (3) Dr Gammon is correct in assuming that leukocyte responsiveness to chemotactins is intact in C5-deficient mice. Peripheral PMNs from C5-deficient (B₁₀D₂/old line) mice respond equally, as well as PMNs from C5-sufficient (B₁₀D² . . . [Full Text PDF of this Article]

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