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Serum bactericidal activity against Neisseria meningitidis in patients with C3 nephritic factors is dependent on IgG allotypes.

Melander Skattum, Lillemor LU ; Gullstrand, Birgitta LU ; Holmström, Eva M LU ; Oxelius, Vivi-Anne LU and Truedsson, Lennart LU (2008) In Clinical Immunology 129. p.123-131
Abstract
The main mechanisms of immune defense against Neisseria meningitidis are serum bactericidal activity (SBA) and opsonophagocytosis. Many complement deficiencies, among them acquired partial C3 deficiency due to stabilizing autoantibodies against the alternative pathway C3 convertase (C3 nephritic factors, C3 NeF); increase the risk of meningococcal infection. SBA against meningococci in patients with C3 NeF was determined along with allelic variants (GM alleles) of the immunoglobulin constant heavy G chain (IGHG) genes. In patients with C3 NeF and in control children, individuals homozygous for G1Mf and G3Mb showed higher SBA against meningococci than heterozygous individuals. Partial complement deficiency in early childhood might explain... (More)
The main mechanisms of immune defense against Neisseria meningitidis are serum bactericidal activity (SBA) and opsonophagocytosis. Many complement deficiencies, among them acquired partial C3 deficiency due to stabilizing autoantibodies against the alternative pathway C3 convertase (C3 nephritic factors, C3 NeF); increase the risk of meningococcal infection. SBA against meningococci in patients with C3 NeF was determined along with allelic variants (GM alleles) of the immunoglobulin constant heavy G chain (IGHG) genes. In patients with C3 NeF and in control children, individuals homozygous for G1Mf and G3Mb showed higher SBA against meningococci than heterozygous individuals. Partial complement deficiency in early childhood might explain the influence of GM variants on SBA in control children. These novel findings imply that the IGHG genotype is important in defense against meningococci in individuals with low complement function and possibly in combination with other immunodeficiencies. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Clinical Immunology
volume
129
pages
123 - 131
publisher
Elsevier
external identifiers
  • wos:000259459200015
  • pmid:18667363
  • scopus:51249123326
ISSN
1521-6616
DOI
10.1016/j.clim.2008.06.010
language
English
LU publication?
yes
id
1accd5d1-942c-4f1f-8f08-2b80e24421e6 (old id 1223675)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18667363?dopt=Abstract
date added to LUP
2008-09-10 11:18:13
date last changed
2017-01-01 07:34:23
@article{1accd5d1-942c-4f1f-8f08-2b80e24421e6,
  abstract     = {The main mechanisms of immune defense against Neisseria meningitidis are serum bactericidal activity (SBA) and opsonophagocytosis. Many complement deficiencies, among them acquired partial C3 deficiency due to stabilizing autoantibodies against the alternative pathway C3 convertase (C3 nephritic factors, C3 NeF); increase the risk of meningococcal infection. SBA against meningococci in patients with C3 NeF was determined along with allelic variants (GM alleles) of the immunoglobulin constant heavy G chain (IGHG) genes. In patients with C3 NeF and in control children, individuals homozygous for G1Mf and G3Mb showed higher SBA against meningococci than heterozygous individuals. Partial complement deficiency in early childhood might explain the influence of GM variants on SBA in control children. These novel findings imply that the IGHG genotype is important in defense against meningococci in individuals with low complement function and possibly in combination with other immunodeficiencies.},
  author       = {Melander Skattum, Lillemor and Gullstrand, Birgitta and Holmström, Eva M and Oxelius, Vivi-Anne and Truedsson, Lennart},
  issn         = {1521-6616},
  language     = {eng},
  pages        = {123--131},
  publisher    = {Elsevier},
  series       = {Clinical Immunology},
  title        = {Serum bactericidal activity against Neisseria meningitidis in patients with C3 nephritic factors is dependent on IgG allotypes.},
  url          = {http://dx.doi.org/10.1016/j.clim.2008.06.010},
  volume       = {129},
  year         = {2008},
}