Evidence map›Paper›PMID 12959222›Full record

ArticleJournal of clinical immunology2003

Immunoglobulin deficiencies and susceptibility to infection among homozygotes and heterozygotes for C2 deficiency.

Chester A Alper, Jianhua Xu, Katherine Cosmopoulos, Brian Dolinski, Rosanne Stein, Gabriel Uko, Charles E Larsen, Devendra P Dubey, Peter Densen, Lennart Truedsson and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of clinical immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Immune responses in neonates.Expert review of clinical immunology · 2014
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Immunoglobulins and complement factor C4 in adult rhinosinusitis.Clinical and experimental immunology · 2006
    Article
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Chester A AlperThe Center for Blood Research, Harvard Medical School, Boston, Massachusetts 02115, USA. alper@cbr.med.harvard.edu
Jianhua Xu
Katherine Cosmopoulos
Brian Dolinski
Rosanne Stein
Gabriel Uko
Charles E Larsen
Devendra P Dubey
Peter Densen
Lennart Truedsson
Gunnar Sturfelt
Anders G Sjöholm
Harvard University · USLund University · SEDana-Farber/Boston Children's Cancer and Blood Disorders Center · USUniversity of Iowa · US

Funding

STUDIES OF NK AND T CELLS IN RELATION TO THE MAJOR HISTOCOMPATIBILITY COMPLEXP01HL029583 · NHLBI · IMMUNE DISEASE INSTITUTE, INC. · PI LARSEN, CHARLES E · 1985 to 2005
$9.8M
INVESTIGATIONS OF HUMAN COMPLEMENTR01AI014157 · NIAID · IMMUNE DISEASE INSTITUTE, INC. · PI ALPER, CHESTER ALLAN · 1985 to 1989
–
INVESTIGATIONS OF HUMAN COMPLEMENTR37AI014157 · NIAID · IMMUNE DISEASE INSTITUTE, INC. · PI ALPER, CHESTER ALLAN · 1990 to 1999
–
NHLBI NIH HHS HL-29583NIAID NIH HHS AI-14157
6 · The paper itself

Abstract

About 25% of C2-deficient homozygotes have increased susceptibility to severe bacterial infections. C2-deficient homozygotes had significantly lower serum levels of IgG2, IgG4, IgD, and Factor B, significantly higher levels of IgA and IgG3 and levels of IgG1 and IgM similar to controls. Type 1 (28 bp deletion in C2 exon 6 on the [HLA-B18, S042, DR2] haplotype or its fragments) and type II (non-type I) C2-deficient patients with increased susceptibility to bacterial infection had significantly lower mean levels of IgG4 (p < 0.04) and IgA (p < 0.01) than those without infections (who had a higher than normal mean IgA level) but similar mean levels of other immunoglobulins and Factor B. Of 13 C2-deficient homozygotes with infections, 85% had IgG4 deficiency, compared with 64% of 25 without infections. IgD deficiency was equally extraordinarily common among infection-prone (50%) and noninfection-prone (70%) homozygous type I C2-deficient patients. IgD deficiency was also common (35%) among 31 type I C2-deficient heterozygotes (with normal or type II haplotypes), but was not found in 5 type II C2-deficient heterozygotes or 1 homozygote. Thus, C2 deficiency itself is associated with many abnormalities in serum immunoglobulin levels, some of which, such as in IgG4 and IgA, may contribute to increased susceptibility to infection. In contrast, IgD deficiency appears not to contribute to increased infections and appears to be a dominant trait determined by a gene or genes on the extended major histocompatibility complex (MHC) haplotype [HLA-B 18, S042, DR2] (but probably not on type II C2-deficient haplotypes) similar to those previously identified on [HLA-B8, SC01, DR3] and [HLA-B18, F1C30, DR3].

Indexed as

Complement C2Complement Factor BDisease SusceptibilityDysgammaglobulinemiaHaplotypesHeterozygoteHomozygoteHumansIgA DeficiencyIgG DeficiencyImmunoglobulin DImmunoglobulinsInfectionsComplement C2Complement Factor BImmunoglobulin DImmunoglobulins

Identifiers

PMID12959222
OpenAlexW1950734237

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.