Activation of Effector Cells of Experimental Allergic Encephalomyelitis in Lewis Rats: Comparison of T-Cell Lines with Primary Cultured Lymph Node Cells

1986 ◽  
Vol 79 (4) ◽  
pp. 370-375 ◽  
Author(s):  
Tadashi Namikawa ◽  
Takashi Yamamura ◽  
Koichiro Sakai ◽  
Tatsuhide Kunishita ◽  
Takeshi Tabira
Keyword(s):  
Lymph Node ◽  
T Cell ◽  
Cell Lines ◽  
Experimental Allergic Encephalomyelitis ◽  
Allergic Encephalomyelitis ◽  
Lewis Rats ◽  
Effector Cells ◽  
Lymph Node Cells ◽  
T Cell Lines ◽  
Experimental Allergic

scholarly journals Transfer of experimental allergic encephalomyelitis in Lewis rats using supernates of incubated sensitized lymph node cells.

1977 ◽  
Vol 145 (5) ◽  
pp. 1405-1410 ◽  
Author(s):  
C C Whitacre ◽  
P Y Paterson
Keyword(s):  
Spinal Cord ◽  
Lymph Node ◽  
Guinea Pig ◽  
Experimental Allergic Encephalomyelitis ◽  
Nervous Tissue ◽  
Allergic Encephalomyelitis ◽  
Lewis Rats ◽  
Transfer Activity ◽  
Lymph Node Cells ◽  
Experimental Allergic

Supernates derived from incubated lymph node cells of Lewis rats sensitized to guinea pig spinal cord-Freund's adjuvant transfer experimental allergic encephalomyelitis (EAE) to syngeneic recipients. EAE supernatant transfer activity (EAE-STA) is not demonstrable in supernates derived from LNC of control donors not sensitized to nervous tissue. After addition of brain antigen to active supernates, EAE-STA is not longer demonstrable.

scholarly journals Protection from experimental allergic encephalomyelitis conferred by a monoclonal antibody directed against a shared idiotype on rat T cell receptors specific for myelin basic protein.

1988 ◽  
Vol 168 (6) ◽  
pp. 2153-2164 ◽  
Author(s):  
M Owhashi ◽  
E Heber-Katz
Keyword(s):  
T Cell ◽  
Myelin Basic Protein ◽  
Experimental Allergic Encephalomyelitis ◽  
Basic Protein ◽  
Specific Cell ◽  
Allergic Encephalomyelitis ◽  
Two Dimensional Gel Electrophoresis ◽  
Lewis Rats ◽  
T Cell Lines ◽  
Experimental Allergic

Immunizing Lewis rats with guinea pig myelin basic protein (MBP) yielded an encephalitogen specific, Ia-restricted, rat-mouse T cell hybridoma 5.10, which was used to establish a clonotypic mAb (10.18) that binds to and precipitates the rat TCR. By two-dimensional gel electrophoresis, the rat TCR was shown to consist of two disulfide-linked peptide chains with mol wt of 48,000 and 39,000. 10.18 binds the majority of cells in MBP-specific T cell lines that are capable of transferring experimental allergic encephalomyelitis (EAE) to Lewis rat recipients, but does not bind to either a purified protein derivative of tuberculin-specific cell line or an OVA-specific line. Furthermore, soluble 10.18 can block antigen-specific stimulation of hybridoma 5.10 but cannot control hybridomas, while immobilized 10.18 stimulates 5.10, but cannot control the hybrids. Though 10.18+ cells are very rare in normal rats, increase of 10.18+ cells is observed in MBP-primed paralyzed rats. Finally, when 10.18 is injected into MBP-primed Lewis rats, EAE is abrogated. We have thus characterized EAE as a "mono-idiotypic" autoimmune disease.

T cell immunity and interferon-γ secretion during experimental allergic encephalomyelitis in Lewis rats

1991 ◽  
Vol 31 (2) ◽  
pp. 165-177 ◽  
Author(s):  
Maha Ibrahim Mustafa ◽  
Per Diener ◽  
Höjeberg Bo ◽  
Peter Van der Meide ◽  
Tomas Olsson
Keyword(s):  
T Cell ◽  
Experimental Allergic Encephalomyelitis ◽  
Interferon Γ ◽  
T Cell Immunity ◽  
Allergic Encephalomyelitis ◽  
Lewis Rats ◽  
Cell Immunity ◽  
Experimental Allergic
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