NDLI: Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity.

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Equine severe combined immunodeficiency: a defect in V(D)J recombination and DNA-dependent protein kinase activity.

Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity.

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An amino acid sequence motif sufficient for subnuclear localization of an arginine/serine-rich splicing factor.

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14-3-3 proteins: potential roles in vesicular transport and Ras signaling in Saccharomyces cerevisiae.

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Microsatellite variability and genetic distances.

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Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lage, A. L. Ma, M. Warren, H. B. Wessels, M. R. Butko, P. Carroll, M. C.
Description	Author Affiliation: Wessels MR ( Channing Laboratory, Brigham and Women's Hospital, Boston, MA, USA.);
Abstract	Group B streptococci (GBS) cause sepsis and meningitis in neonates and serious infections in adults with underlying chronic illnesses. Specific antibodies have been shown to be an important factor in protective immunity for neonates, but the role of serum complement is less well defined. To elucidate the function of the complement system in immunity to this pathogen, we have used the approach of gene targeting in embryonic stem cells to generate mice totally deficient in complement component C3. Comparison of C3-deficient mice with mice deficient in complement component C4 demonstrated that the 50% lethal dose for GBS infection was reduced by approximately 50-fold and 25-fold, respectively, compared to control mice. GBS were effectively killed in vitro by human blood leukocytes in the presence of specific antibody and C4-deficient serum but not C3-deficient serum. The defective opsonization by C3-deficient serum in vitro was corroborated by in vivo studies in which passive immunization of pregnant dams with specific antibodies conferred protection from GBS challenge to normal and C4-deficient pups but not C3-deficient pups. These results indicate that the alternative pathway is sufficient to mediate effective opsonophagocytosis and protective immunity to GBS in the presence of specific antibody. In contrast, the increased susceptibility to infection of non-immune mice deficient in either C3 or C4 implies that the classical pathway plays an essential role in host defense against GBS infection in the absence of specific immunity.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	25
Volume Number	92
Language	English
Publisher	National Academy of Sciences
Publisher Date	1995-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Complement C3 Deficiency Complement C4 Immunity Streptococcal Infections Immunology Streptococcus Agalactiae Pathogenicity Animals Animals, Newborn Antibodies, Bacterial Genetics Disease Susceptibility Immunity, Active Immunity, Innate Immunity, Maternally-Acquired Leukocytes Mice Opsonin Proteins Phagocytosis Pregnancy Pathology Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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