Suppression of Experimental Allergic Encephalomyelitis by Transfer of Lymph Node Cells from Lewis Rats Pretreated with Complete Freund’s Adjuvant

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A single injection of complete Freund’s adjuvant blended with aluminum hydroxide gel (ALU-CFA) was successfully used to prevent clinical as well as histologic experimental allergic encephalomyelitis (EAE) in Lewis rats for more than 330 days. Adjuvant preparations with Mycobacterium tuberculosis were more potent than those with Mycobacterium butyricum. Neither the removal of the ALU-CFA inoculum nor a splenectomy 1 month after immunization arrested the adjuvant induced unresponsiveness. However cyclophosphamide restored responsiveness in more than half of the treated animals when applied 2 days before the encephalitogenic challenge at a dose of 20 mg/kg. Passive EAE was not prevented by the ALU-CFA pretreatment. The disease was induced by the transfer of 4 × 10⁶ T lymphocytes of a cell line reactive against myelin basic protein. This indicates that the adjuvant prevents EAE at the inductive rather than at the effector phase of the autoimmune response.

Section: Resultsmentioning

confidence: 99%

“…However, it is an open question whether or not CFA has an EAE preventive effect in rats as well. Though there were only minor differences in the experimental protocols protection [8,32] as well as full susceptibility [13,31] were found.…”

Section: Introductionmentioning

confidence: 99%

Unresponsiveness to Experimental Allergic Encephalomyelitis in Lewis Rats Pretreated with Complete Freund’s Adjuvant

Hempel¹,

A²,

Freitag³

et al. 1985

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“…There is ample evidence that pretreat ment with complete Freund's adjuvant (CFA) pre vents EAE in guinea pigs [16] and rats [12]. Unrespon siveness after pretreatment with CFA is regarded as cell-mediated because it is transferred by lymph node cells [10] and abrogated by low doses of cyclophos phamide [12].…”

Section: Introductionmentioning

confidence: 99%

Protection against Experimental Allergic Encephalomyelitis with Complete Freund’s Adjuvant Is Unaffected by Prostaglandin Synthesis Inhibition

Weber

Hempel²

1989

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Pretreatment with complete Freund’s adjuvant blended with aluminium hydroxide (ALU-CFA) prevents the clinical as well as histological manifestation of experimental allergic encephalomyelitis (EAE) in Lewis rats. Suppression of prostaglandin biosynthesis with the cyclooxygenase inhibitor piroxicam (10 mg/kg body weight) from day 2 before to day 17 after EAE induction could not restore responsiveness in pretreated animals. In contrast piroxicam increased ALU-CFA-induced suppression of autoantibodies against myelin basic protein. In controls not pretreated with ALU-CFA, clinical signs of EAE were attenuated by piroxicam, whereas mononuclear infiltration of the brain remained unchanged. Therefore it is unlikely that prostaglandins exert an important function in the regulation of immune responses in this model of autoimmunity.

“…In the present experiment 1 animal displayed a mild clinical EAE and in another case histological alterations of EAE could be detected. Because in more than 100 experi ments of this type complete unresponsiveness was found [10,14], we suggest that in these 2 cases protec tion might have been incomplete for unknown techni cal reasons.…”

Section: Resultsmentioning

confidence: 88%

“…It could be transferred by lymph node cells to untreated syngenic animals [10]. Suppressor cells are also involved in the unresponsiveness of rats convalescent from EAE [16] and in tolerance against EAE achieved by pretreatment with GpBP [22].…”

Section: Discussionmentioning

confidence: 99%

Protection against Experimental Allergic Encephalomyelitis with Complete Freund’s Adjuvant Is Unaffected by Ionizing Irradiation

Weber¹,

Hempel²

1987

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Long-lasting resistance to experimental allergic encephalomyelitis (EAE) was obtained in Lewis rats either by an immunization with complete Freund’s adjuvant blended with aluminum hydroxide (ALU-CFA) or by convalescence from EAE. Total body irradiation at a dose of 500 R given both 1 day after ALU-CFA (or disease induction) and EAE challenge did not abrogate the protection. No antibodies against myelin basic protein could be detected in irradiated animals. In contrast high antibody titers were measured in non-irradiated controls recovered from EAE and subsequently resistant to the disease. Therefore it is unlikely that antibodies against myelin basic proteins are of any importance in protection from EAE. The studies suggest that unspecific radioresistant suppressor cells play a role in resistance to EAE.