Complement and the Major Histocompatibility Systems

  • Casper Jersild
  • Pablo Rubinstein
  • Noorbibi K. Day
Part of the Comprehensive Immunology book series (COMIMUN, volume 2)


Hereditary deficiencies of specific components of the complement (C) system were first discovered in experimental animals (Moore, 1919; Coca, 1920; Hyde, 1923) and later in man (Klemperer et al., 1966). These isolated C deficiencies have been of importance for the understanding of the functional interrelationships between the various C components and in elucidating the biological significance of this complex system. Inherited deficiencies, among other possibilities, may be the outcome of genetically determined defects resulting in any one of the following: (1) total absence of synthesis of one or more of the polypeptides that make up the biologically active component due to the lack of function of either a structural or a regulator gene; (2) the production of a functionally inactive component due to a structural gene defect; or (3) the continuous synthesis or constitutive derepression of a specific inhibitor. Irrespective of which mechanism(s) mentioned is the basis for each specific deficiency, we shall denote genes resulting in deficient C components as C° genes; e.g., C2° is a C2-deficient gene.


Major Histocompatibility Complex Hereditary Deficiency Mixed Leukocyte Culture Hereditary Angioneurotic Edema Histocompatibility System 
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Copyright information

© Plenum Publishing Corporation 1977

Authors and Affiliations

  • Casper Jersild
    • 1
  • Pablo Rubinstein
    • 2
  • Noorbibi K. Day
    • 3
  1. 1.Tissue Typing Laboratory, Blood Bank and Blood Grouping DepartmentUniversity Hospital (Rigshospitalet)CopenhagenDenmark
  2. 2.Kimball Research Institute of the New York Blood CenterNew YorkUSA
  3. 3.Sloan-Kettering Institute for Cancer ResearchNew YorkUSA

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