Eugene M. Hoenig

Passive Transfer Of Allergic Encephalomyelitis Between Inbred Rat Strains: Correlation With Transplantation Antigens

Experimental allergic encephalomyelitis (EAE) was elicited in donor Lewis rats by immunization with heterologous spinal cord antigen and adjuvants. Suspensions of cells from their draining lymph nodes transferred the disease passively to normal isohistogenic Lewis recipients and to genetically tolerant (Lewis X BN) or (Lewis X Buffalo)F1 hybrids, in all of which Lewis cells should enjoy extended survival. However, in accordance with the rules of transplantation genetics responsible for homograft rejection, transfers of such Lewis cells to normal BN, Buffalo, ACI and Wistar/Furth recipients were not effective, nor were transfers of cells from immunized hybrid donors to normal Lewis recipients. Donor cells would not be expected to survive in these situations. On the other hand, transfers of immmunized Lewis cells to Fischer 344 recipients were successful, especially after adrenalectomy of recipients or focal impairment of their blood-brain barrier by cyanide treatment. This inter-strain transfer of EAE was attributed to genetic identity of these two strains at a major histocompatibility locus, and was obtained despite differences at minor histocompatibility loci. There was no evidence of a significant Y-linked histocompatibility factor in this system.

Allergic Encephalomyelitis: Passive Transfer Prevented by Encephalitogen

Allergic encephalomyelitis was produced in rats by passive transfer of lymph node cells from donors immunized intradernmally with nleural tissute or an encephalitogenic basic protein pluts adjulvants. The same basic protein, injected intravenously into the recipients before or after transfer of lymph node cells, prevented the disease. Even established lesions were reversed. Inhibition by basic protein was specific for encephalomyelitis; it had no effect onz passive transfer of allergic adrenalitis.

Altered distribution of lesions after repeated passive transfers of allergic encephalomyelitis.

Summary Repeated attacks of experimental allergic encephalomyelitis (EAE) were induced in rats by 2, 3 or 4 consecutive biweekly passive transfers of living, encephalitogenic, lymphoid cells. The incidence and severity of clinical signs of EAE decreased progressively during successive attacks. A decrease in spinal cord lesions was found histologically only after the fourth transfer. Unexpectedly, the cerebellum revealed a marked increase of EAE lesions after the second, third or fourth transfers. This redistribution of lesions may be due to local blockade at the sites of original attack in the spinal cord.

Three Localized forms of Experimental Allergic Encephalomyelitis: An Ultrastructural Comparison

Ordinary, hyperacute and neutrophilic forms of experimental allergic encephalomyelitis (EAE) were compared by electron microscopy. All 3 forms were produced by passive transfer and were localized to the cerebral cortex of the Lewis rat at the periphery of a heat injury. All forms were characterized by perivascular cuffs of mononuclear cells around capillaries and venules, infiltration by inflammatory cells, including neutrophils, of the adjoining parenchyma, enlargement of perivascular and parenchymal extracellular spaces, edema and fibrin deposition. Basophils were identified for the first time within the lesions and the adjacent parenchyma of all 3 forms and within the lesions of both active and passively transferred allergic adrenalitis, an analogous autoimmune disease. While all 3 forms of EAE shared common features, perivascular mononuclear cell cuffing of vessels in ordinary EAE, fibrin deposition and edema in hyperacute EAE, and polymorphonuclear leukocytes in neutrophilie EAE were quantitatively exaggerated, distinguishing the 3 forms. Greatly enlarged interendothelial cell junctions appeared to be a unique feature of localized, passively transferred hyperacute EAE.

Fine structure of contrasting choroid plexus lesions caused by tertiary amines or cyclophosphamide.

Hydropic alterations of the fine structure of the choroid plexus epithelium following administration of three different tertiary amines to rats were compared with alterations produced by cyclophosphamide and with normal choroid plexus. Single doses of 2, 7-bis(2-(diethylamino)-ethoxy)- 4− methyl-1,8-naphtyridine HCI or 2,6,-di-(omega-dimethyl aminoethoxy)-pyridine produced dramatic accumulations of membrane-limited vacuoles. Multiple doses of 2,7-bis-(diethylaminoethoxy) fluoren-9-one HC1 (tilorone) produced accumulations of dense cytoplasmic bodies in choroid epithelia cells in addition to the hydropic vacuoles. Differential responses to these agents suggested functional specialization or temporal variation in function among adjacent choroidal cells. Despite the occurrence of pronounced plasma exudation in the plexitis following cyclophosphamide treatment, there was no hydropic vacuolization.

Allergic encephalomyelitis: passive transfer across major histocompatibility barrier.

Summary Passive transfer of allergic encephalomyelitis by injection of living, immunized lymph node cells into normal recipients constitutes a graft of lymphoid cells. It has been accomplished previously when histocompatibility barriers were absent, minor, or undefined. Treatment with an immunosuppressive drug and cells bearing donor-type antigens has now made passive transfer possible despite differences in major transplantation antigens between Lewis donor and BN recipient rats.