An immunohistological study of autoimmune encephalomyelitis and neuritis in the rabbit: Observations in the dorsal root ganglion using the freeze-dried paraffin-embedded tissue technique

Previous studies of experimental autoimmune encephalomyelitis have shown that, in the central nervous system, the emigration of T-lymphocytes precedes that of mononuclear phagocytes during inflammatory lesion formation. In the present report, the formation of analogous lesions of autoimmune neuritis...

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Published inJournal of the neurological sciences Vol. 83; no. 2; pp. 293 - 304
Main Authors Simmons, R.D., Buzbee, T.M., Linthicum, D.S.
Format Journal Article
LanguageEnglish
Published Shannon Elsevier B.V 01.02.1988
Elsevier Science
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Summary:Previous studies of experimental autoimmune encephalomyelitis have shown that, in the central nervous system, the emigration of T-lymphocytes precedes that of mononuclear phagocytes during inflammatory lesion formation. In the present report, the formation of analogous lesions of autoimmune neuritis (EAN) was investigated in the dorsal root ganglia of rabbits immunized with homologous spinal cord in Freund's adjuvant. The relative time course of emigration of T-lymphocytes and mononuclear phagocytes into the ganglia was examined using monoclonal antibody labeling of both types of cells in serial sections of freeze-dried paraffin-embedded tissue. Results indicate that, unlike in the central nervous system, in the rabbit dorsal root ganglion T-lymphocytes and mononuclear phagocytes appear to emigrate simultaneously, as revealed by their concomitant presence in the earliest detectable lesions of EAN. It was also found that the cortical region of the rabbit dorsal root ganglion was a preferential site of EAN lesion formation, and that such lesions correlated well with the onset of clinical signs of paralysis. These results are discussed within the context of known “blood-tissue barriers” and the possible local modulation of inflammatory cell entry into regions of the nervous system.
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ISSN:0022-510X
1878-5883
DOI:10.1016/0022-510X(88)90076-7