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| 2. |
- Strigård, Karin, et al.
(författare)
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Elimination of CD8+ T cells in vivo does not break induced immunospecific tolerance to experimental allergic neuritis in rats.
- 1988
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Ingår i: Scandinavian Journal of Immunology. - 0300-9475 .- 1365-3083. ; 28:3, s. 325-330
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Tidskriftsartikel (refereegranskat)abstract
- The role of CD8+ T 'cytotoxic/suppressor' T cells in induced immunospecific tolerance and during recovery after actively induced disease was examined by means of elimination of CD8+ cells from Lewis rats using in vivo treatment by Ox8 monoclonal antibodies, in experimental allergic neuritis (EAN). Animals depleted of CD8+ T cells after recovery from EAN did not show any clinical signs of relapse. Other animals were pretreated with the peripheral nerve basic protein P2 and thereby rendered resistant to disease induction with a potentially neuritogenic emulsion. The elimination of CD8+ T cells did not result in EAN here either. Thus, the CD8+ T-cell population does not seem to participate in the suppression of this autoimmune disease under these experimental conditions.
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| 3. |
- Strigård, Karin, et al.
(författare)
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In vivo monoclonal antibody treatment with Ox19 (anti-rat CD5) causes disease relapse and terminates P2-induced immunospecific tolerance in experimental allergic neuritis.
- 1989
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Ingår i: Journal of Neuroimmunology. - 0165-5728 .- 1872-8421. ; 23:1, s. 11-18
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Tidskriftsartikel (refereegranskat)abstract
- The role of CD5+ lymphocytes in the recovery phase and on immunospecific protection against experimental allergic neuritis (EAN) was examined in Lewis rats by in vivo treatment with Ox19, a mouse anti-rat CD5 monoclonal antibody. Animals pretreated with the peripheral nerve basic protein P2 and thereby rendered resistant to the disease showed clinical signs of EAN after intraperitoneal (i.p.) Ox19 injection given at the same time as the rechallenge with neuritogenic doses of myelin in Freund's complete adjuvant. Non-pretreated rats recovered from signs of EAN developed a clinical relapse after i.p. Ox19 injections. Taken together, these data suggest an important regulatory role of the CD5 receptor in the immune response.
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| 4. |
- Strigård, Karin, et al.
(författare)
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In vivo treatment of rats with monoclonal antibodies against gamma interferon : effects on experimental allergic neuritis.
- 1989
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Ingår i: Acta Neurologica Scandinavica. - 0001-6314 .- 1600-0404. ; 80:3, s. 201-207
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Tidskriftsartikel (refereegranskat)abstract
- To elucidate the role of gamma interferon in experimental allergic neuritis (EAN) a mouse monoclonal antibody (DB-1) directed against rat gamma interferon was used to treat rats during different phases of the development of experimental allergic neuritis (EAN). The effects of this treatment were followed by clinical evaluation, and in some instances by immunohistochemical analysis of lymphoid organs and affected nerves for presence of MHC class II antigens and various T cell subsets. DB-1 treatment given after onset of clinical symptoms (Day 15 after immuniozation with myelin) shortened disease duration, compared with non-treated EAN controls. Affected nerves of DB-1 treated animals showed reduced expression of MHC class II antigens and lower numbers of T lymphocytes within the affected nerves. In contrast, when DB-1 treatment was given on the day of immunization (Day 0), the disease duration increased, and when given before onset of the disease (Day 9) the clinical course was not significantly affected. The results support an important role for gamma interferon in the pathogenesis of EAN.
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| 5. |
- Strigård, Karin, et al.
(författare)
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Modulation of experimental allergic neuritis in rats by in vivo treatment with monoclonal anti T cell antibodies.
- 1988
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Ingår i: Journal of the Neurological Sciences. - 0022-510X .- 1878-5883. ; 83:2-3
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Tidskriftsartikel (refereegranskat)abstract
- Monoclonal antibodies (MCA) to different T lymphocyte cell surface antigens have been used to treat rats during different phases of the development of experimental allergic neuritis (EAN). The effects of this treatment were followed by clinical evaluation and in some instances by immunohistochemical analysis of lymphoid organs and affected nerves of the antibody-treated rats. Several MCA, W3/13 (pan T cell reactive), W3/25 (anti-rat CD4), Ox 8 (anti-rat CD8) as well as Ox 6 (anti-Ia) partly prevented clinical signs of EAN when given shortly before expected onset of disease, whereas W3/13 and Ox 8 given at the height of disease did not further affect disease development. However, Ox 19 (anti-rat CD5) given at the same time as immunization partly prevented clinical signs of EAN, while Ox 19 given shortly before expected onset of disease or during height of disease drastically exaggerated disease symptoms. Immunohistochemical studies after Ox 8 or Ox 19 treatment showed a complete absence of staining for the respective antibodies, while staining was preserved with the other MCA. It is concluded that: (1) Ox 8 positive "suppressor/cytotoxic" T lymphocytes do not exert any suppressive effects on EAN during the now investigated phases of disease, and that (2) anti T lymphocyte antibodies (here Ox 19) may exert opposite effects on autoimmune disease when given at different phases of disease development. This may have implications for potential therapeutic trials of MCA therapy for putative autoimmune demyelinating diseases in man.
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| 6. |
- Strigård, Karin, et al.
(författare)
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T-lymphocyte subsets, functional deficits, and morphology in sciatic nerves during experimental allergic neuritis
- 1987
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Ingår i: Muscle and Nerve. - New York : John Wiley & Sons. - 0148-639X .- 1097-4598. ; 10:4, s. 329-337
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Tidskriftsartikel (refereegranskat)abstract
- Conduction velocities, demyelination, "macrophage/dendritic" cells, different sets of T-lymphocytes, and immunoglobulins were estimated in sciatic nerves during various phases of experimental allergic neuritis in Lewis rats. Demyelination was minimal day 15 postimmunization (p.i.) when conduction velocity already was reduced, somewhat more pronounced day 17 p.i. when nerve conduction was blocked, and most pronounced day 23 p.i. when nerve conduction partially had recovered. This suggests a dissociation between the degree of demyelination and the functional deficits. Decrease of sciatic nerve conduction velocities coincided with endoneurial appearance of T-lymphocytes and "macrophage/dendritic" cells, as well as endoneurial immunoglobulins, day 15 p.i. Later partial functional recovery occurred in parallel with the disappearance of T-cells. The degree of functional deficits thus correlated with the number of endoneurial T-lymphocytes. T-cells may, directly or indirectly, initiate several of the disease components in experimental allergic neuritis, including the nerve conduction deficit.
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