Humoral response to herpes simplex virus is complement-dependent.
The complement system represents a cascade of serum proteins, which provide a major effector function in innate immunity. Recent studies have revealed that complement links innate and adaptive immunity via complement receptors CD21/CD35 in that it enhances the B cell memory response to noninfectious protein antigens introduced i.v. To examine the importance of complement for immune responses to virus infection in a peripheral tissue, we compared the B cell memory response of mice deficient in complement C3, C4, or CD21/CD35 with wild-type controls. We found that the deficient mice failed to generate a normal memory response, which is characterized by a reduction in IgG antibody and germinal centers. Thus, complement is important not only in the effector function of innate immunity but also in the stimulation of memory B cell responses to viral-infected cell antigens in both blood and peripheral tissues.
Da Costa
X J
XJ
Department of Microbiology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.
Brockman
M A
MA
Alicot
E
E
Ma
M
M
Fischer
M B
MB
Zhou
X
X
Knipe
D M
DM
Carroll
M C
MC
D000818:Animals; D000914:Antibodies, Viral / Q000096:biosynthesis*; D001402:B-Lymphocytes / Q000276:immunology; D003165:Complement System Proteins / Q000502:physiology*; D006561:Herpes Simplex / Q000276:immunology; D018259:Herpesvirus 1, Human / Q000276:immunology*; D007156:Immunologic Memory; D051379:Mice; D013601:T-Lymphocytes / Q000276:immunology; D001616:beta-Galactosidase / Q000276:immunology
D000914:Antibodies, Viral; D003165:Complement System Proteins; D001616:beta-Galactosidase