Analysis of T cell receptor ? chains in the rat: I. Allelic polymorphism of V?8.2 is not a predisposing genetic factor in susceptibility to experimental allergic encephalomyelitis

Gold, Daniel P.; Schroder, Kim; Mueller, Deanna; Wilson, Darcy B.

doi:10.1002/(sici)1097-4547(19960915)45:6<700::aid-jnr6>3.0.co;2-c

Cited by 2 publications

(1 citation statement)

References 25 publications

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“…In this regard, our findings demonstrating the conversion of the relatively EAEresistant F344 rat strain to a susceptible one with L-NIL are reminiscent of the findings of Krakowski and Owens [25]. Recent studies from our laboratory in EAE ( [26], D. P. Gold, unpublished observations) and from others in experimental autoimmune uveoretinitis [27] have come to the common conclusion that F344 rats are capable of generating potential pathogenic cells following autoantigen challenge, but that the activity of the cells can only be demonstrated following adoptive transfer. Further studies will be needed to elucidate where NO is playing a role in blocking the pathogenic capacity of these cells.…”

Section: Discussionsupporting

confidence: 78%

Nitric oxide and the immunomodulation of experimental allergic encephalomyelitis

et al. 1997

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Previous studies examining the effect of nitric oxide synthase (NOS) inhibition on the course of experimental allergic encephalomyelitis (EAE) have yielded conflicting results. This may relate to the use of nonspecific inhibitors and to differences between active and adoptive EAE. We examined the effect of treatment with L-N-(1-iminoethyl)lysine (L-NIL), a selective inhibitor of the cytokine-inducible isoform of NOS, on the clinical course of active and adoptive EAE in Lewis rats. We find that while L-NIL treatment of recipients is protective in adoptive EAE, treatment of active EAE with L-NIL leads to a marked accentuation of disease expression. In L-NIL-treated animals treated with myelin basic protein/complete Freund's adjuvant (MBP/CFA), disease onset is accelerated and clinical symptoms are more severe. Accentuation of integrated disease scores is seen even if L-NIL treatment is started 5 days following immunization. The histological findings in involved spinal cords from L-NIL-treated animals with active EAE are similar to those from untreated animals with similar clinical scores. L-NIL treatment of MBP/CFA-immunized animals does not prevent recovery from clinical symptoms, nor does it allow for reinduction of disease in animals previously immunized with MBP/CFA. Treatment of F344 rats, a strain which is relatively nonsusceptible for EAE, with L-NIL results in consistent evidence of EAE following immunization with MBP/CFA. These findings, together with our previous work on interstitial nephritis, support a role for endogenously generated NO in immunoregulation of T cell responses following immunization with antigen in CFA, and suggest that inducibility of NOS expression may be an important susceptibility factor for autoimmunity.

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Section: Discussionsupporting

confidence: 78%

Nitric oxide and the immunomodulation of experimental allergic encephalomyelitis

et al. 1997

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Contrasting contributions of complementarity-determining region 2 and hypervariable region 4 of rat BV8S2+ (V 8.2) TCR to the recognition of myelin basic protein and different types of bacterial superantigens

Kreiß

Asmuss²,

Krejci³

et al. 2004

International Immunology

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In experimental autoimmune encephalomyelitis (EAE) of LEW rats, BV8S2(+) (V(beta)8.2) T cells dominate the RT1B(l)-restricted response to guinea pig myelin basic protein (gpMBP), and respond to the superantigens (SAg) Staphylococcus enterotoxin C1 (SEC1), Mycoplasma arthritidis SAg (MAS) and Yersinia pseudotuberculosis mitogen (YPM). T cells expressing the closely related BV8S4 differ from BV8S2 T cells in their response to gpMBP, and the SAg SEC1 and MAS, but not in their response to YPM. The functional differences between BV8S2 and BV8S4, which vary in complementarity-determining/hypervariable region 4 (CDR4/HV4) and CDR2, were analyzed by cloning and mutating a TCR with features typical for gpMBP-specific BV8S2(+) TCR. The wild-type BV8S2 receptor and the BV8S4-like CDR2 + 4beta double mutant of BV8S2 showed the same differences in ligand specificity as polyclonal BV8S2(+) and BV8S4(+) lymphocyte populations. The CDR2beta mutant lost its reactivity for SEC1 and gpMBP(68-88), but the CDR4/HV4beta mutation abolished only activation by SEC1. Thus, CDR2 and HV4 contribute not only differently to recognition of peptide antigens, but also to recognition of different types of bacterial SAg.

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Analysis of T cell receptor ? chains in the rat: I. Allelic polymorphism of V?8.2 is not a predisposing genetic factor in susceptibility to experimental allergic encephalomyelitis

Cited by 2 publications

References 25 publications

Nitric oxide and the immunomodulation of experimental allergic encephalomyelitis

Nitric oxide and the immunomodulation of experimental allergic encephalomyelitis

Contrasting contributions of complementarity-determining region 2 and hypervariable region 4 of rat BV8S2+ (V 8.2) TCR to the recognition of myelin basic protein and different types of bacterial superantigens

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