Gene transfer through the blood–nerve barrier: NGF-engineered neuritogenic T lymphocytes attenuate experimental autoimmune neuritis

Kramer, Rainer; Zhang, Yiping; Gehrmann, Jochen; Gold, Ralf; Thoenen, H.; Wekerle, Hartmut

doi:10.1038/nm1195-1162

Cited by 79 publications

(37 citation statements)

References 18 publications

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“…Mice were maintained according to approved Home Office protomental allergic neuritis. 28 Quantitative studies should be performed using purcols and following Institute guidelines. The number of mice used in these studies was the minimum required to ified arthritogenic T cell clones or lines that could be characterized in vitro where the number of cells transachieve statistical significance in this study.…”

Section: Figure 6 Tgf ␤1 Inhibits Gelatinase Activity In Inflamed Pawmentioning

confidence: 99%

Pathogenic lymphoid cells engineered to express TGF β1 ameliorate disease in a collagen-induced arthritis model

Chernajovsky¹,

Adams²,

Triantaphyllopoulos³

et al. 1997

Gene Ther

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Collagen-induced arthritis in DBA/1 mice is a model of paw swelling and higher levels of anti-collagen antibody. rheumatoid arthritis with marked synovitis and erosions.By infecting arthritogenic splenocytes ex vivo with TGF ␤1 The disease can be adoptively transferred to SCID mice retrovirus, this exacerbation was inhibited. TGF ␤1 was with arthritogenic splenocytes from DBA/1 mice injected effective in lowering inflammation of joints with already with bovine collagen type II. However, infection of arthritoestablished arthritis and inhibiting the spreading of the disgenic splenocytes with a retrovirus expressing TGF ␤1 ease to other joints. Transient reduction in anti-collagen inhibits development of arthritis in SCID mice. When DBA/1 antibody levels could also be obtained using purified T cells mice, at onset of arthritis have additional arthritogenic infected with TGF ␤1 retrovirus. In addition, expression of splenocytes transferred, exacerbation occurs, reflected in TGF ␤1 in lymphocytes reduced the levels of gelatinase a rapid increase in the number of arthritic joints, increased (MMP2) activity in inflamed joints.

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Section: Figure 6 Tgf ␤1 Inhibits Gelatinase Activity In Inflamed Pawmentioning

confidence: 99%

Pathogenic lymphoid cells engineered to express TGF β1 ameliorate disease in a collagen-induced arthritis model

Chernajovsky¹,

Adams²,

Triantaphyllopoulos³

et al. 1997

Gene Ther

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“…Intriguing results have already been obtained in inbred rodent models of arthritis, 87 neuritis, 88 and encephalomyelitis. 78 However, it is still an open question whether this approach will be feasible in the genetically heterogeneous human population.…”

Section: Future Developmentsmentioning

confidence: 74%

Gene therapy in nonhuman primate models of human autoimmune disease

et al. 2003

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Before autoimmune diseases in humans can be treated with gene therapy, the safety and efficacy of the used vectors must be tested in valid experimental models. Monkeys, such as the rhesus macaque or the common marmoset, provide such models. This publication reviews the state of the art in monkey models for rheumatoid arthritis and multiple sclerosis and the (few) gene therapy experiments that have been performed in these models. Gene Therapy (2003) 10, 890-901.

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“…Tissue-specific targeting using gene therapy-transduced autoreactive T cells reinfused into the host as the delivery vehicle has also been proposed (5,8). Tissue-protective strategies currently under investigation include efforts aimed at remyelinating lost neural tissue by using nerve-specific autoimmune T lymphocytes as vehicles to deliver therapeutically useful neurotrophic factors across the endothelial blood-nerve barrier (28), or healing thermal injuries by delivering growth factor genes (29). The use of inducible vector systems, such as the ones containing a doxycycline-response element, may be useful to limit the expression of the transgene for a defined time period (30).…”

Section: The Future Of Antigen-specific Gene Therapymentioning

confidence: 99%