Abstract
Inoculation of mice with the granulocyte-depleting monoclonal antibody RB6-8C5 showed that neutrophils are critical protective effector cells during a Chlamydia trachomatis infection. In addition, administration of monoclonal antibody 2E6 demonstrated that extravasation of neutrophils into the peritoneal cavity in response to inoculation with the C. trachomatis MoPn biovar is dependent on the surface beta-2 integrin molecule CD18.
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