Passive Transfer of ‘Allergic’ Encephalomyelitis with Antibrain Serum injected into the Lateral Ventricle of the Brain

Oligodendrocyte-specific expression and autoantigenicity of transaldolase in multiple sclerosis.

“…A breakdown of the blood brain barrier may provide a route of entry for otigodendrocyte-specific antibodies. Likewise, antibodies to TAL-H may mediate demyelination by attracting microglia and macrophage through their Fc receptors and, thus, triggering phagocytosis and antibody-dependent cell-mediated cytotoxicity (41). Antibodies to TAL-H were detected in a subset of patients with MS.…”

Transformation of Rodent Lymphoid Cells by an Encephalitogen of Human Origin

“…There has been much controversy over the relative importance of antibody or cellular media tion of immunologic injury in the pathogenesis of these diseases, and evidence for both has been discovered. For the following reasons, the weight of opinion at the present time is that cellular hypersensitivity is the primary contributor in EAE: (1) EAE has only been transferred once with serum, and that by the distinctly unphysiologic means of repeated intraventricular injections through an indwelling cannula [12]; (2) it is readily transferred with one inoculum of sensitized lymphoid cells [22]; (3) its development is impaired by neonatal thymectomy, a procedure known to reduce delayed, or cellular hypersensitivity reactions more than the antibody response [11]; (4) the production of EAE in the burscctomizcd, irradiated chicken, which makes no circulating antibody, is no more difficult than in the normal chicken [3]; (5) the onset of disease does not correlate with appearance of complement-fixing antibodies [21] but very well indeed with delayed hypersensitivity as determined by skin testing [24]; (6) injections of encephalitogen in Freund's incomplete adjuvant can protect guinea pigs from subsequent encephalitogenic challenge, or can suppress EAE in those already challenged [1], and a similar protection is obtained in Wistar rats by administering serum from animals recovering from EAE [23]; and (7) doses of anti-lymphocyte serum which suppress delayed hypersensitivity reactions but not circulating antibody titers in guinea pigs inhibit the development of EAE [27].…”

Transfer of Lesions of Allergic Encephalomyelitis in Sheep with Cell‐Free Lymph from Animals Sensitized with Homologous Spinal Cord plus Adjuvant

“…Perhaps the most compelling evidence that EAE is cell-mediated and dependent on T cells derives from studies showing that disease can be transferred from sensitized donors to naive recipients with Iymphoid cells [7,10] and that removal of T cells from the cell population [2] abrogates transfer. As a corollary, the strongest evidence against antibodies playing a role in causation of disease is the consistent inability to transfer disease passively with sera from sensitized animals [3] except under extreme conditions [5].…”