Combined homozygous factor H and heterozygous C2 deficiency in an Italian family. 1988

M Brai, and G Misiano, and S Maringhini, and I Cutaja, and G Hauptmann
Institute of General Pathology, University of Palermo, Italy.

Three of four children in a family have homozygous (less than 1% of normal) deficiency of factor H of the complement system and both parents, who are first cousins, are heterozygous for the same defect. The father and two of the H-deficient siblings also have a partial C2 deficiency. One of the children with combined deficiencies is affected by systemic lupus erythematosus with nephritis. No increased susceptibility to infections has been observed in the family. H deficiency is inherited in an autosomal codominant manner and is independently transmitted from C2 deficiency and HLA haplotypes. In the homozygous state it is associated with very low serum concentrations of B and C3, barely demonstrable as activated molecules. C5 is greatly reduced (less than 5%). Also, properdin and C6-9 are decreased. The findings in this family demonstrate that the occurrence of systemic lupus erythematosus in one of the children affected by a combined deficiency of factor H and C2 raises the question whether this pathology is related to the complete factor H or to the heterozygous C2 deficiency. Complete H deficiency is not necessarily accompanied by overt illness.

UI MeSH Term Description Entries
D007122 Immunoelectrophoresis A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.
D008040 Genetic Linkage The co-inheritance of two or more non-allelic GENES due to their being located more or less closely on the same CHROMOSOME. Genetic Linkage Analysis,Linkage, Genetic,Analyses, Genetic Linkage,Analysis, Genetic Linkage,Genetic Linkage Analyses,Linkage Analyses, Genetic,Linkage Analysis, Genetic
D008180 Lupus Erythematosus, Systemic A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow. Libman-Sacks Disease,Lupus Erythematosus Disseminatus,Systemic Lupus Erythematosus,Disease, Libman-Sacks,Libman Sacks Disease
D010375 Pedigree The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition. Family Tree,Genealogical Tree,Genealogic Tree,Genetic Identity,Identity, Genetic,Family Trees,Genealogic Trees,Genealogical Trees,Genetic Identities,Identities, Genetic,Tree, Family,Tree, Genealogic,Tree, Genealogical,Trees, Family,Trees, Genealogic,Trees, Genealogical
D011415 Complement Factor B A glycine-rich, heat-labile serum glycoprotein that contains a component of the C3 CONVERTASE ALTERNATE PATHWAY (C3bBb). Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb. C3 Proactivator,C3PA,Complement 3 Proactivator,Factor B,Properdin Factor B,Bb Fragment of Factor B,Complement Factor B Fragment, Bb,Complement Factor B, Alternative Pathway,Complement Factor B-Derived Fragment Bb,Complement Factor Ba,Complement Factor Bb,Complement Protein B,Complement Protein Factor B,Properdin Factor Ba,Properdin Factor Bb,Properdin Factor Bf,Properdin Factor Bf F1,Bb, Complement Factor,Complement Factor B Derived Fragment Bb,Factor B, Complement,Factor B, Properdin,Factor Ba, Complement,Factor Ba, Properdin,Factor Bb, Complement,Factor Bb, Properdin,Factor Bf, Properdin,Proactivator, C3,Proactivator, Complement 3,Protein B, Complement
D002648 Child A person 6 to 12 years of age. An individual 2 to 5 years old is CHILD, PRESCHOOL. Children
D003175 Complement C2 A component of the CLASSICAL COMPLEMENT PATHWAY. C2 is cleaved by activated COMPLEMENT C1S into COMPLEMENT C2B and COMPLEMENT C2A. C2a, the COOH-terminal fragment containing a SERINE PROTEASE, combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE). C2 Complement,Complement 2,Complement Component 2,C2, Complement,Complement, C2,Component 2, Complement
D003179 Complement C3b The larger fragment generated from the cleavage of COMPLEMENT C3 by C3 CONVERTASE. It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. C3b participates in IMMUNE ADHERENCE REACTION and enhances PHAGOCYTOSIS. It can be inactivated (iC3b) or cleaved by various proteases to yield fragments such as COMPLEMENT C3C; COMPLEMENT C3D; C3e; C3f; and C3g. C3b Complement,C3bi,Complement 3b,Complement Component 3b,Inactivated C3b,iC3b,C3b, Complement,C3b, Inactivated,Complement, C3b,Component 3b, Complement
D003180 Complement C3b Inactivator Proteins Endogenous proteins that inhibit or inactivate COMPLEMENT C3B. They include COMPLEMENT FACTOR H and COMPLEMENT FACTOR I (C3b/C4b inactivator). They cleave or promote the cleavage of C3b into inactive fragments, and thus are important in the down-regulation of COMPLEMENT ACTIVATION and its cytolytic sequence. C3b Inactivators,C3b Inhibitors,Complement 3b Inactivators,Complement 3b Inhibitors,Complement C3b Inactivators,Complement C3b Inhibitor Proteins,Conglutinogen Activating Factors,Factors, Conglutinogen Activating,Inactivators, C3b,Inactivators, Complement 3b,Inactivators, Complement C3b,Inhibitors, C3b,Inhibitors, Complement 3b
D005260 Female Females

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