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Restricted immunoglobulin constant heavy G chain genes in primary immunodeficiencies.

Oxelius, Vivi-Anne LU ; Ochs, Hans D and Hammarström, Lennart (2008) In Clinical Immunology 128. p.190-198
Abstract
Some primary immunodeficiencies (PIDs) express low serum levels of antibodies. The constant heavy G chain (IGHG) genes, also representing Fc domains of gamma3, gamma1 and gamma2 on chromosome 14q32.3, genotyped by the alternative IgG subclass allotypes, found in four fixed IGHG haplotypes, designating four B cell variants, were identified by a competitive ELISA and double immunodiffusion. IGHG genes were hypothesized to contribute to the development of PIDs. From 235 Caucasian patients, the homozygous IGHGbf-n/bf-n diplotype (B(bf-n)/B(bf-n) cells) dominated significantly in 43 IgG2 deficiency (OR 6.0), 32 common variable immunodeficiency (OR 4.6) and 22 Ataxia telangiectasia (OR 3.0) and the IGHGga-n/ga-n diplotype (B(ga-n)/B(ga-n) cells)... (More)
Some primary immunodeficiencies (PIDs) express low serum levels of antibodies. The constant heavy G chain (IGHG) genes, also representing Fc domains of gamma3, gamma1 and gamma2 on chromosome 14q32.3, genotyped by the alternative IgG subclass allotypes, found in four fixed IGHG haplotypes, designating four B cell variants, were identified by a competitive ELISA and double immunodiffusion. IGHG genes were hypothesized to contribute to the development of PIDs. From 235 Caucasian patients, the homozygous IGHGbf-n/bf-n diplotype (B(bf-n)/B(bf-n) cells) dominated significantly in 43 IgG2 deficiency (OR 6.0), 32 common variable immunodeficiency (OR 4.6) and 22 Ataxia telangiectasia (OR 3.0) and the IGHGga-n/ga-n diplotype (B(ga-n)/B(ga-n) cells) dominated in 53 IgG3 deficiency (OR 10.6) and 21 Wiscott-Aldrich syndrome (OR 4.1). 62 IgA deficiency patients were dominated by both diplotypes (OR 2.3 and OR 2.8 respectively). Restricted IGHG genes, restricted IgG allotypes (Fc domains) and restricted B cells are significant in PIDs for diagnosis, treatment and pathogenetic mechanisms. (Less)
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author
; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Clinical Immunology
volume
128
pages
190 - 198
publisher
Elsevier
external identifiers
  • wos:000257941400009
  • pmid:18502179
  • scopus:46949099168
ISSN
1521-6616
DOI
10.1016/j.clim.2008.03.520
language
English
LU publication?
yes
id
7045b12f-b96e-41b2-be96-e23898a7c6a5 (old id 1153791)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18502179?dopt=Abstract
date added to LUP
2016-04-04 08:43:05
date last changed
2022-01-29 03:53:42
@article{7045b12f-b96e-41b2-be96-e23898a7c6a5,
  abstract     = {{Some primary immunodeficiencies (PIDs) express low serum levels of antibodies. The constant heavy G chain (IGHG) genes, also representing Fc domains of gamma3, gamma1 and gamma2 on chromosome 14q32.3, genotyped by the alternative IgG subclass allotypes, found in four fixed IGHG haplotypes, designating four B cell variants, were identified by a competitive ELISA and double immunodiffusion. IGHG genes were hypothesized to contribute to the development of PIDs. From 235 Caucasian patients, the homozygous IGHGbf-n/bf-n diplotype (B(bf-n)/B(bf-n) cells) dominated significantly in 43 IgG2 deficiency (OR 6.0), 32 common variable immunodeficiency (OR 4.6) and 22 Ataxia telangiectasia (OR 3.0) and the IGHGga-n/ga-n diplotype (B(ga-n)/B(ga-n) cells) dominated in 53 IgG3 deficiency (OR 10.6) and 21 Wiscott-Aldrich syndrome (OR 4.1). 62 IgA deficiency patients were dominated by both diplotypes (OR 2.3 and OR 2.8 respectively). Restricted IGHG genes, restricted IgG allotypes (Fc domains) and restricted B cells are significant in PIDs for diagnosis, treatment and pathogenetic mechanisms.}},
  author       = {{Oxelius, Vivi-Anne and Ochs, Hans D and Hammarström, Lennart}},
  issn         = {{1521-6616}},
  language     = {{eng}},
  pages        = {{190--198}},
  publisher    = {{Elsevier}},
  series       = {{Clinical Immunology}},
  title        = {{Restricted immunoglobulin constant heavy G chain genes in primary immunodeficiencies.}},
  url          = {{http://dx.doi.org/10.1016/j.clim.2008.03.520}},
  doi          = {{10.1016/j.clim.2008.03.520}},
  volume       = {{128}},
  year         = {{2008}},
}