Experimental autoimmune encephalomyelitis in "low" and "high" interleukin 2 producer rats. I. Cellular basis of induction.
Albino Oxford (AO) rats in comparison to the Dark August (DA) strain exhibit lower susceptibility to the induction of experimental autoimmune encephalomyelitis (EAE), and interleukin 2 (IL-2) production by their spleen and lymph node cells is significantly lower. The cellular analysis of these differences in the outcome of the EAE induction, possibly related to the differences in the IL-2 production, revealed different changes in the T cell subsets in the draining lymph node (DLN) and different cellular composition of the mononuclear infiltrates in the central nervous system (CNS). After the encephalitogenic challenge, the frequency of CD8+ T cells was much higher and the expansion of CD4+ T cells was much lower in the DLN of "low" IL-2 producer rats. AO rats have not shown any clinical sign of EAE, although histological lesions in the early phases of EAE (Day 7-9) were similar to those seen in diseased DA rats. CD4/CD8 T cell ratios and the number of cells bearing receptor for IL-2 (IL-2-R+ cells) and cells bearing class II MHC antigens (Ia+) were significantly lower in the mononuclear cell infiltrates of AO rats. These data are compatible with the notion that CD4+ IL-2-R+ encephalitogenic T cells induce clinical signs of EAE in susceptible animals and show that CD8+ T cells are present in a higher percentage in the lesions of the symptom-free AO rats.
Vukmanović
S
S
Institute of Microbiology and Immunology, School of Medicine, University of Belgrade, Yugoslavia.
Mostarica Stojković
M
M
Lukić
M L
ML
D000818:Animals; D002490:Central Nervous System / Q000473:pathology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000473:pathology; D005260:Female; D007376:Interleukin-2 / Q000096:biosynthesis*; D010641:Phenotype; D051381:Rats; D015375:Receptors, Interleukin-2 / Q000032:analysis; D013601:T-Lymphocytes / Q000145:classification
D007376:Interleukin-2; D015375:Receptors, Interleukin-2