Abstract
At the beginning of the nineteenth century, knowledge of immunity was limited to a few practical methods based on empirical observations, e.g., the observation by Jenner in 1798 that inoculation with cowpox material induced an immunity to smallpox. The discoveries by Louis Pasteur and Robert Koch that microorganisms caused fermentations and were responsible for a number of infectious diseases, greatly advanced the concepts of susceptibility and immunity in a limited number of diseases. In the late nineteenth century, the complement system was discovered by Fodor(1887), Nuttall(1888), and Buchner (1889a, b) through studying the bactericidal action of blood serum. It was recognized that killing of bacteria in fresh serum required at least two different substances: a heat-stable (30 min, 56 °C) factor, today known to be the antibody specific for the particular microorganism; and a heat-labile factor, which was normally present in each serum. This factor was at first termed “alexine” (Buchner 1889a, b) and later designated “complement” (Pfeiffer and Issaeff 1894; Bordet 1896). On 18 May 1889, Buchner made the following Statement at a lecture in Munich: “Das Vorhandensein bakterienfeindlicher Wirkungen durch flüssige Bestandthile der Körpersäfte lässt die überall nachweisbare Thätigkeit der Phagozyten als weniger ausschlaggebend erkennen” (The presence of bactericidal action in body fluids reveals the overall detectable activity of phagocytes as less decisive). This statement by the chief advocate of the humoral theory of resistance to microbial infections was directed against the cellular theory of immunity proposed by Metchnikoff. In his answer to Buchner’s critique, Metchnikoff (1889; English translation 1905) came to the conclusion, based on his own work, that “the postulates of this theory are often not in accord with the real facts,” and that the bactericidal effect of body fluids has nothing in common with the phenomenon of immunity („la propriété bactéricide des humeurs ne correspond nullement aux phénomènes de l’immunité“).
Alexine is nothing but a leucocytic product
Elie Metchnikoff, 1905
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Abbreviations
- ATEe:
-
N-acetyl-L-tyrosine ethyl ester
- Con A:
-
concanavalin A
- CRP:
-
C-reactive protein
- C1 INH:
-
C1 inhibitor
- DEAE:
-
diethylaminoethyl
- DFP:
-
diisopropyl fluorophosphate
- DNP:
-
dinitrophenyl
- DNP-HSA:
-
dinitrophenylated human serum albumin
- DS:
-
dextran sulfate
- EDTA:
-
ethylenediaminetetraacetate
- E-TNP:
-
trinitrophenylated erythrocyte
- FCS:
-
fetal calf serum
- FITC:
-
fluorescein isothioeyanate
- GPS:
-
guinea pig serum
- HSA:
-
human serum albumin
- Ig:
-
immunoglobulin
- LPS:
-
bacterial-derived lipopolysaccharide
- M 199:
-
medium 199
- NaCl:
-
sodium chloride
- NPGB:
-
p-nitrophenyl-p′ -guanidinobenzoate
- PA:
-
polyanion
- PBS:
-
phosphate-buffered saline
- PS:
-
ant venom-derived polysaccharide
- RB 200:
-
lissamine rhodamine B
- Sp54:
-
pentosan polysulfo ester
- PVS:
-
polyvinyl sulfate
- SDS PAGE:
-
sodium dodecyl sulfate polyacrylamide gel electrophoresis
- SRBC:
-
sheep red blood cell
- TAMe:
-
N-tosyl-L-arginine methyl ester
- TNP:
-
trinitrophenyl
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Ghebrehiwet B (1981) Clq inhibitor (ClgINH): Functional properties and possible relationship to a lymphocyte membrane-associated Clq precipitin. J Immunol 126:1837–1842
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Golan MD, Hitschold T, Loos M (1981) The reconstitution of human Cl, the first complement component. Binding of Clr and Cls to Clq influences the Clq conformation. FEBS Lett 128:281–285
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© 1983 Springer-Verlag Berlin Heidelberg
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Loos, M. (1983). Biosynthesis of the Collagen-like C1q Molecule and its Receptor Functions for Fc and Polyanionic Molecules on Macrophages. In: Cooper, M., et al. Current Topics in Microbiology and Immunology. Current Topics in Microbiology and Immunology, vol 102. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-68906-2_1
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