Literature DB >> 10072635

Reference typing report for complement component C4.

G Mauff1, B Luther, P M Schneider, C Rittner, B Stradmann-Bellinghausen, R Dawkins, J M Moulds.   

Abstract

During the 7th Complement Genetics Workshop, Mainz, Germany, May 1998, a complement component C4 typing exercise took place with the aim of applying present technologies to the definition of reference C4 alleles/phenotypes and the recognition of nonexpressed (Q0) C4 alleles within expressed haplotypes. Eleven samples were submitted from 3 laboratories and tested by 14 participating laboratories with basic protein-typing technologies; in addition, each laboratory contributed data from local expertise. The samples were introduced to the reference typing for one or more characteristic allotype or for partial or total nonexpression of one isotype. The blinded samples were centrally evaluated and the results discussed among the participants at a plenum meeting. From the results, the samples could be classified into a group of common, easy to diagnose pheno-/allotypes, less common but still unanimously recognised variants, and a third group with difficult pheno-/allotypes. Within the latter group, the allotypes were either new (C4A '92'; C4B '93') and/or showed partial or total reversed antigenicity and unusual Rodgers/Chido (Rg/Ch) PCR subtypes (C4A '92'; C4A 12; C4B '35'; C4B '13'). Semiquantitative C4-alpha-chain estimates of relative isotype levels correlated well with the number of alleles seen at each locus by agarose gel electrophoresis, and were superior to other isotype quantitation methods. From the evaluation of the reference typing it was concluded that the recognition of rare, aberrant or hybrid C4 alleles with partial or total reversed Rg/Ch antigenicity or monoclonal reactivity is still difficult in most instances; besides isotype-dependent lysis, relative migration values, immunoblots with Rg- and Ch-specific monoclonal antibodies, Rg/Ch PCR typing, side-by-side comparison with already described allotypes will ultimately be required. The recognition of nonexpressed alleles within C4A and C4B expressed phenotypes remains the major obstacle in C4 genetic typing. Finally, a conclusive interpretation of DNA typing results will be achieved only in the context of complete allotyping results at the protein level, and at present cannot replace conventional protein allotyping.

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Year:  1998        PMID: 10072635     DOI: 10.1159/000019079

Source DB:  PubMed          Journal:  Exp Clin Immunogenet        ISSN: 0254-9670


  13 in total

1.  Defining targets for complement components C4b and C3b on the pathogenic neisseriae.

Authors:  Lisa A Lewis; Sanjay Ram; Alpana Prasad; Sunita Gulati; Silke Getzlaff; Anna M Blom; Ulrich Vogel; Peter A Rice
Journal:  Infect Immun       Date:  2007-11-05       Impact factor: 3.441

2.  Determining the one, two, three, or four long and short loci of human complement C4 in a major histocompatibility complex haplotype encoding C4A or C4B proteins.

Authors:  Erwin K Chung; Yan Yang; Kristi L Rupert; Karla N Jones; Robert M Rennebohm; Carol A Blanchong; C Yung Yu
Journal:  Am J Hum Genet       Date:  2002-09-10       Impact factor: 11.025

3.  Genetic sophistication of human complement components C4A and C4B and RP-C4-CYP21-TNX (RCCX) modules in the major histocompatibility complex.

Authors:  Erwin K Chung; Yan Yang; Robert M Rennebohm; Marja-Liisa Lokki; Gloria C Higgins; Karla N Jones; Bi Zhou; Carol A Blanchong; C Yung Yu
Journal:  Am J Hum Genet       Date:  2002-09-11       Impact factor: 11.025

Review 4.  Phenotypes, genotypes and disease susceptibility associated with gene copy number variations: complement C4 CNVs in European American healthy subjects and those with systemic lupus erythematosus.

Authors:  Y L Wu; Y Yang; E K Chung; B Zhou; K J Kitzmiller; S L Savelli; H N Nagaraja; D J Birmingham; B P Tsao; B H Rovin; L A Hebert; C Y Yu
Journal:  Cytogenet Genome Res       Date:  2009-03-11       Impact factor: 1.636

5.  Molecular basis of complete complement C4 deficiency in two North-African families with systemic lupus erythematosus.

Authors:  Y L Wu; G Hauptmann; M Viguier; C Y Yu
Journal:  Genes Immun       Date:  2009-03-12       Impact factor: 2.676

6.  Genetic deficiency of complement isoforms C4A or C4B predicts improved survival of metastatic renal cell carcinoma.

Authors:  Ghazal I Zafar; Elizabeth A Grimm; Wei Wei; Marcella M Johnson; Julie A Ellerhorst
Journal:  J Urol       Date:  2009-01-16       Impact factor: 7.450

7.  Gene copy-number variation and associated polymorphisms of complement component C4 in human systemic lupus erythematosus (SLE): low copy number is a risk factor for and high copy number is a protective factor against SLE susceptibility in European Americans.

Authors:  Yan Yang; Erwin K Chung; Yee Ling Wu; Stephanie L Savelli; Haikady N Nagaraja; Bi Zhou; Maddie Hebert; Karla N Jones; Yaoling Shu; Kathryn Kitzmiller; Carol A Blanchong; Kim L McBride; Gloria C Higgins; Robert M Rennebohm; Robert R Rice; Kevin V Hackshaw; Robert A S Roubey; Jennifer M Grossman; Betty P Tsao; Daniel J Birmingham; Brad H Rovin; Lee A Hebert; C Yung Yu
Journal:  Am J Hum Genet       Date:  2007-04-26       Impact factor: 11.025

Review 8.  Of mice and men: the relevance of the mouse to the study of human SLE.

Authors:  D J Birmingham; B H Rovin; C Y Yu; L A Hebert
Journal:  Immunol Res       Date:  2001       Impact factor: 4.505

9.  Complement-4 deficiency in a child with systemic lupus erythematosus presenting with standard treatment-resistant severe skin lesion.

Authors:  Betul Sozeri; Sevgi Mir; Afig Berdeli
Journal:  ISRN Rheumatol       Date:  2011-02-10

Review 10.  Role of MHC-linked susceptibility genes in the pathogenesis of human and murine lupus.

Authors:  Manfred Relle; Andreas Schwarting
Journal:  Clin Dev Immunol       Date:  2012-06-19
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