THE Guillain-Barré syndrome (GBS) is an acute polyneuropathy of humans characterized histologically by mononuclear cell infiltrates and segmental demyelination.1-3 Although described initially by Landry4 in 1859, and Guillain et al5 in 1916, the etiology and pathogenesis of this important disorder still remain unknown. In 1955, Waksman and Adams6 described a peripheral neuropathy in animals, experimental allergic neuritis (EAN), produced by the injection of peripheral nervous tissue in complete Freund's adjuvant. Because of the similar clinical and pathologic features in this immune-mediated experimental disease, and the GBS, a common mechanism of tissue injury was postulated.
Recent studies have shown that increased numbers of atypical basophilic mononuclear cells, many of which are synthesizing DNA, occur in peripheral blood during immune reactions.7-9 These circulating sensitized cells, or immunocytes, are presumed to mirror the intense concomitant proliferation occurring in the host's lymphoid tissues. Circulating immunocytes have also
Cook SD, Dowling PC, Whitaker JN. The Guillain-Barré Syndrome: Relationship of Circulating Immunocytes to Disease Activity. Arch Neurol. 1970;22(5):470–474. doi:10.1001/archneur.1970.00480230088011
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