Summary
The three main immunoglobulin classes obey the basic principles of passive protein transfer at the blood-CSF barrier and the serum-derived portions could therefore be quantified with the help of the permeability marker albumin. The Ig fractions secreted into the CSF by sessile plasma cell clones have been determined in various inflammatory diseases of the central nervous system. The humoral immune response in multiple sclerosis and chronic encephalitis of unknown cause was dominated by IgG antibodies. In most other inflammatory diseases IgA and IgM were concomitantly synthesized, e.g. in neurosyphilis and meningoencephalitis caused by viruses of the herpes group. In tick-borne meningopolyneuritis Bannwarth, only IgM and in bacterial meningitis only IgA may be produced locally. The detection of a secretory immunoglobulin fraction in the CSF may be the sole laboratory parameter in chronic inflammatory processes of the nervous system.
Zusammenfassung
Die drei Immunglobulin-Klassen G, A und M befolgen die Gesetze des passiven Proteintransfers an der Blut-Liquor-Schranke. Deshalb können die aus dem Serum stammenden Anteile mit Hilfe des Permeabilitäts-markers Albumin quantifiziert werden. Die IgG-Fraktionen, die durch gewebsständige Plasmazell-Klone bei verschiedenen entzündlichen Erkrankungen des Zentralnervensystems in den Liquor abgegeben werden, konnten quantitativ bestimmt werden. Bei der multiplen Sklerose und der chronischen Encephalitis ungeklärter Ursache wird überwiegend IgG synthetisiert. Bei den meisten anderen entzündlichen Erkrankungen wird zur gleichen Zeit auch IgA und IgM gebildet, etwa bei der Neurolues und der Herpes-Encephalitis. Bei der durch Zecken übertragenen Meningo-Polyneuritis Bannwarth wird gelegentlich nur IgM und bei der bakteriellen Meningitis nur IgA synthetisiert. Eine lokal gebildete Immunglobulin-Fraktion kann der einzige klinisch-chemische Parameter für das Vorliegen einer chronisch-entzündlichen Erkrankung des Nervensystems sein.
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Felgenhauer, K. Differentiation of the humoral immune response in inflammatory diseases of the central nervous system. J Neurol 228, 223–237 (1982). https://doi.org/10.1007/BF00313413
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DOI: https://doi.org/10.1007/BF00313413