The influence of cyclosporin A on T cell activation, cytokine gene expression and cell-mediated immunity

Thomson, Angus W.; Duncan, J. I.

doi:10.1007/978-94-009-0859-8_4

Cited by 15 publications

(10 citation statements)

References 138 publications

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“…CsA was used for autoimmune disease. It had a significant effect on immune depression [17]. In this study CsA was used as the positive reference substance in vitro and in vivo models.…”

Section: Preparation Of Physalin Hmentioning

confidence: 99%

Investigation of the immunosuppressive activity of Physalin H on T lymphocytes

Sun

et al. 2010

International Immunopharmacology

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“…CsA was used for autoimmune disease. It had a significant effect on immune depression [17]. In this study CsA was used as the positive reference substance in vitro and in vivo models.…”

Section: Preparation Of Physalin Hmentioning

confidence: 99%

Investigation of the immunosuppressive activity of Physalin H on T lymphocytes

Sun

et al. 2010

International Immunopharmacology

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“…chain of the ^l-integrin very lale antigen family). We have also examined lhe influence of cyclosporin A (CsA), a powerful inhibitor of CD4^ T cell activation and cytokine production (Thomson & Duncan. 1989;Granelli-Piperno.…”

Section: Introductionmentioning

confidence: 99%

Adhesion molecule expression in psoriatic skin lesions and the influence of cyclosporin A

Horrocks

Duncan

Oliver

et al. 1991

Clinical and Experimental Immunology

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SUMMARYNormal skin of healthy individuals and bolh lesional and uninvolved skin from patienis with psoriasis before and after receiving cyciosporin A (CsA; 25 or 5 mg/kg per day) was examined by immunocytochemislry for differences in expression of adhesion-relevanl epitopes. Normal, lesional and uninvolved skin all showed staining of basal keratinocyiesfor CD29 {the common/i chain of the /JI -integrin family). No other adhesion molecule investigated was detected on structural components of normal skin. In uninvolved skin, weak expression of CD54 (intercellular adhesion molecule I. ICAM-1) was noted on vascular endothelium. Uninvolved keralinocytes were found to stain with anti-CD58 {kucocyte function-associated antigen 3, LFA-3) and there was weak expression of CD 11 b (a chain of complement C3bi receptor) and CD 11 c (a chain of p 150., 95 molecule) bul not CDl la (leucocyte function-associated antigen 1. LFA-I, a chain) on those celts. In icsional skin, in addition to expression of CD58. there was also enhanced expression of CD 11 c. Weak expression of CD54 on keratinocytes was also observed. Lesional blood vessels were found to stain strongly with anti-CD54. CD29 and CD58. CDI la was expressed only on infiltrating mononuclear celts. CsA treatment produced marked clinical improvement, accompanied by the loss of CD54 expression on keralinoeytes. However, despite the loss of T celts from lesionat skin with CsA treatment. CD54 persisted on blood vessels. CsA was found to have no effect on keratinocyte expression of CD29. CD58orCDl Ibandc. ThepersisteneeofCD54on vascular endothetium and of adhesion molecule expression on keratinocytes. despite resolution of the skin lesions, may explain the universal and rapid recurrence of psoriasis on cessation of CsA administration.

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“…Cyclosporin A (CsA) has powerful effects on cell-mediated immunity, especially on helper T cells (Thomson and Webster, 1988). CsA reduces interleukin 2 (IL-2) production and reduces the expression of IL-2 receptors by lymphocytes (Prince and John, 1986).…”

Section: Introductionmentioning

confidence: 99%

The effects of prophylactic cyclosporin A on experimental allergic neuritis (EAN) in the Lewis rat. Induction of relapsing EAN using low dose cyclosporin A

McCombe

Kreek

Pender

1990

Journal of Neuroimmunology

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Experimental allergic neuritis (EAN) was induced in Lewis rats by inoculation with bovine intradural root myelin plus adjuvants. Animals treated with high dose (30 mg/kg) cyclosporin A (CsA) 3 times per week did not develop clinical EAN during the period of CsA treatment, but had an episode of EAN after cessation of CsA treatment. Animals treated with low dose (4 mg/kg) CsA 3 times per week developed EAN during the period of treatment, and after cessation of CsA treatment all of these animals developed relapsing EAN with disease continuing for up to four episodes. In contrast, 30-40% of untreated animals had a mild second episode of EAN but no further attacks. Histological studies performed in treated and untreated animals at the time of clinical episodes revealed inflammation and demyelination in the spinal roots and dorsal root ganglia. When animals were challenged with a second inoculation at age 7 months, one of 15 untreated control animals but none of the CsA treated animals developed an episode of EAN.

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The influence of cyclosporin A on T cell activation, cytokine gene expression and cell-mediated immunity

Cited by 15 publications

References 138 publications

Investigation of the immunosuppressive activity of Physalin H on T lymphocytes

Investigation of the immunosuppressive activity of Physalin H on T lymphocytes

Adhesion molecule expression in psoriatic skin lesions and the influence of cyclosporin A

The effects of prophylactic cyclosporin A on experimental allergic neuritis (EAN) in the Lewis rat. Induction of relapsing EAN using low dose cyclosporin A

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