|
|
||||||||
From the Department of Pediatrics, Emory University School of Medicine, Atlanta, Georgia 30303, and the Center for Disease Control, Public Health Service, United States Department of Health, Education and Welfare, Atlanta, Georgia 30333
Abstract
Human peripheral blood mononuclear cells which mediate antibody-dependent cellular cytotoxicity (ADCC) against herpes simplex virus- (HSV) infected target cells consist of both adherent (MA) and nonadherent (MNA) effector cell populations. These two cell populations can be distinguished by their different phagocytic properties and morphologic appearance, their requirement for antibody in the ADCC reaction, and the rapidity with which they lyse target cells in the presence of immune serum. The MA cells are predominantly phagocytic and have the morphologic characteristics of monocyte-macrophages, whereas the MNA cells are nonphagocytic and appear to be small to medium-sized lymphocytes. Optimal expression of ADCC by MA cells requires higher concentrations of immune serum than does MNA cell-mediated ADCC. MA-mediated cell killing is first detectable by 8 hr and reaches completion after 24 hr of incubation. In contrast, MNA-mediated ADCC produces target cell damage by 2 hr and reaches completion at 8 hr of incubation. Unlike MNA effector cells, the MA effector cells are profoundly inhibited after preincubation with either latex or silica particles. The HSV immune status of the donor had no effect on the ability of either cell population to mediate ADCC.
These data demonstrate the participation of both nonadherent mononuclear cells, presumably K cells, and monocyte-macrophages, in ADCC directed against HSV-infected target cells.
Footnotes
1 This work was supported in part by National Cancer Institute fellowships 1 F32 CA05232, and 1 F22 CA00577-01, by Contract CP 433393 from the National Cancer Institute, by Grant 5 RO 1-DE 03924 from the National Institute of Dental Research and by Training Program AI 00447-04 of National Institute of Allergy and Infectious Disease, National Institutes of Health, Public Health Service.
2 S. K.'s current address is Program in Infectious Diseases and Clinical Microbiology. The University of Texas Health Science Center at Houston, 6400 West Cullen Street, Houston Texas, 77030.
This article has been cited by other articles:
![]() |
J.-I. Sin, V. Ayyavoo, J. Boyer, J. Kim, R. B. Ciccarelli, and D. B. Weiner Protective immune correlates can segregate by vaccine type in a murine herpes model system Int. Immunol., November 1, 1999; 11(11): 1763 - 1773. [Abstract] [Full Text] [PDF] |
||||
![]() |
J.-I. Sin, J. J. Kim, R. L. Arnold, K. E. Shroff, D. McCallus, C. Pachuk, S. P. McElhiney, M. W. Wolf, S. J. Pompa-de Bruin, T. J. Higgins, et al. IL-12 Gene as a DNA Vaccine Adjuvant in a Herpes Mouse Model: IL-12 Enhances Th1-Type CD4+ T Cell-Mediated Protective Immunity Against Herpes Simplex Virus-2 Challenge J. Immunol., March 1, 1999; 162(5): 2912 - 2921. [Abstract] [Full Text] [PDF] |
||||
![]() |
J.-I. Sin, J. J. Kim, J. D. Boyer, R. B. Ciccarelli, T. J. Higgins, and D. B. Weiner In Vivo Modulation of Vaccine-Induced Immune Responses toward a Th1 Phenotype Increases Potency and Vaccine Effectiveness in a Herpes Simplex Virus Type 2 Mouse Model J. Virol., January 1, 1999; 73(1): 501 - 509. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |