Cytokine production in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis: dynamics of mRNA expression for interleukin-10, interleukin-12, cytolysin, tumor necrosis factor alpha and tumor necrosis factor beta.

Shohreh Issazadeh-Navikas; A Ljungdahl; B Höjeberg; M Mustafa; T Olsson

Cytokine production in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis: dynamics of mRNA expression for interleukin-10, interleukin-12, cytolysin, tumor necrosis factor alpha and tumor necrosis factor beta.

Shohreh Issazadeh-Navikas, A Ljungdahl, B Höjeberg, M Mustafa, T Olsson

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

170 Citationer (Scopus)

Abstract

Udgivelsesdato: 1995-Sep

Originalsprog	Engelsk
Tidsskrift	Journal of Neuroimmunology
Vol/bind	61
Udgave nummer	2
Sider (fra-til)	205-12
Antal sider	7
ISSN	0165-5728
Status	Udgivet - 1995

Bibliografisk note

Keywords: Animals; Encephalomyelitis, Autoimmune, Experimental; Gene Expression; In Situ Hybridization; Interleukin-10; Interleukin-12; Lymphotoxin-alpha; Male; Membrane Glycoproteins; Perforin; Pore Forming Cytotoxic Proteins; RNA, Messenger; Rats; Rats, Inbred Lew; Spinal Cord; Tumor Necrosis Factor-alpha

Citationsformater

Issazadeh-Navikas, S., Ljungdahl, A., Höjeberg, B., Mustafa, M., & Olsson, T. (1995). Cytokine production in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis: dynamics of mRNA expression for interleukin-10, interleukin-12, cytolysin, tumor necrosis factor alpha and tumor necrosis factor beta. Journal of Neuroimmunology, 61(2), 205-12.

Cytokine production in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis: dynamics of mRNA expression for interleukin-10, interleukin-12, cytolysin, tumor necrosis factor alpha and tumor necrosis factor beta. / Issazadeh-Navikas, Shohreh; Ljungdahl, A; Höjeberg, B et al.
I: Journal of Neuroimmunology, Bind 61, Nr. 2, 1995, s. 205-12.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

Issazadeh-Navikas, S, Ljungdahl, A, Höjeberg, B, Mustafa, M & Olsson, T 1995, 'Cytokine production in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis: dynamics of mRNA expression for interleukin-10, interleukin-12, cytolysin, tumor necrosis factor alpha and tumor necrosis factor beta.', Journal of Neuroimmunology, bind 61, nr. 2, s. 205-12.

Issazadeh-Navikas, Shohreh ; Ljungdahl, A ; Höjeberg, B et al. / Cytokine production in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis: dynamics of mRNA expression for interleukin-10, interleukin-12, cytolysin, tumor necrosis factor alpha and tumor necrosis factor beta. I: Journal of Neuroimmunology. 1995 ; Bind 61, Nr. 2. s. 205-12.

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title = "Cytokine production in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis: dynamics of mRNA expression for interleukin-10, interleukin-12, cytolysin, tumor necrosis factor alpha and tumor necrosis factor beta.",

abstract = "The kinetics of mRNA expression in the central nervous system (CNS) for a series of putatively disease-promoting and disease-limiting cytokines during the course of experimental autoimmune encephalomyelitis (EAE) in Lewis rats were studied. Cytokine mRNA-expressing cells were detected in cryosections of spinal cords using in situ hybridization technique with synthetic oligonucleotide probes. Three stages of cytokine mRNA expression could be distinguished: (i) interleukin (IL)-12, tumor necrosis factor (TNF)-beta (= lymphotoxin-alpha) and cytolysin appeared early and before onset of clinical signs of EAE; (ii) TNF-alpha peaked at height of clinical signs of EAE; (iii) IL-10 appeared increasingly at and after clinical recovery. The early expression of IL-12 prior to the expression of interferon-gamma (IFN-gamma) mRNA shown previously is consistent with a role of IL-12 in promoting proliferation and activation of T helper 1 (Th1) type cells producing IFN-gamma. The TNF-beta mRNA expression prior to onset of clinical signs favours a role for this cytokine in disease initiation. A pathogenic effector role of TNF-alpha was suggested from these observations that TNF-alpha mRNA expression roughly paralleled the clinical signs of EAE. This may be the case also for cytolysin. IL-10-expressing cells gradually increased to high levels in the recovery phase of EAE, consistent with a function in down-regulating the CNS inflammation. From these data we conclude that there is an ordered appearance of putative disease-promoting and -limiting cytokines in the CNS during acute monophasic EAE.",

author = "Shohreh Issazadeh-Navikas and A Ljungdahl and B H{\"o}jeberg and M Mustafa and T Olsson",

note = "Keywords: Animals; Encephalomyelitis, Autoimmune, Experimental; Gene Expression; In Situ Hybridization; Interleukin-10; Interleukin-12; Lymphotoxin-alpha; Male; Membrane Glycoproteins; Perforin; Pore Forming Cytotoxic Proteins; RNA, Messenger; Rats; Rats, Inbred Lew; Spinal Cord; Tumor Necrosis Factor-alpha",

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T1 - Cytokine production in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis: dynamics of mRNA expression for interleukin-10, interleukin-12, cytolysin, tumor necrosis factor alpha and tumor necrosis factor beta.

AU - Issazadeh-Navikas, Shohreh

AU - Ljungdahl, A

AU - Höjeberg, B

AU - Mustafa, M

AU - Olsson, T

N1 - Keywords: Animals; Encephalomyelitis, Autoimmune, Experimental; Gene Expression; In Situ Hybridization; Interleukin-10; Interleukin-12; Lymphotoxin-alpha; Male; Membrane Glycoproteins; Perforin; Pore Forming Cytotoxic Proteins; RNA, Messenger; Rats; Rats, Inbred Lew; Spinal Cord; Tumor Necrosis Factor-alpha

PY - 1995

Y1 - 1995

N2 - The kinetics of mRNA expression in the central nervous system (CNS) for a series of putatively disease-promoting and disease-limiting cytokines during the course of experimental autoimmune encephalomyelitis (EAE) in Lewis rats were studied. Cytokine mRNA-expressing cells were detected in cryosections of spinal cords using in situ hybridization technique with synthetic oligonucleotide probes. Three stages of cytokine mRNA expression could be distinguished: (i) interleukin (IL)-12, tumor necrosis factor (TNF)-beta (= lymphotoxin-alpha) and cytolysin appeared early and before onset of clinical signs of EAE; (ii) TNF-alpha peaked at height of clinical signs of EAE; (iii) IL-10 appeared increasingly at and after clinical recovery. The early expression of IL-12 prior to the expression of interferon-gamma (IFN-gamma) mRNA shown previously is consistent with a role of IL-12 in promoting proliferation and activation of T helper 1 (Th1) type cells producing IFN-gamma. The TNF-beta mRNA expression prior to onset of clinical signs favours a role for this cytokine in disease initiation. A pathogenic effector role of TNF-alpha was suggested from these observations that TNF-alpha mRNA expression roughly paralleled the clinical signs of EAE. This may be the case also for cytolysin. IL-10-expressing cells gradually increased to high levels in the recovery phase of EAE, consistent with a function in down-regulating the CNS inflammation. From these data we conclude that there is an ordered appearance of putative disease-promoting and -limiting cytokines in the CNS during acute monophasic EAE.

AB - The kinetics of mRNA expression in the central nervous system (CNS) for a series of putatively disease-promoting and disease-limiting cytokines during the course of experimental autoimmune encephalomyelitis (EAE) in Lewis rats were studied. Cytokine mRNA-expressing cells were detected in cryosections of spinal cords using in situ hybridization technique with synthetic oligonucleotide probes. Three stages of cytokine mRNA expression could be distinguished: (i) interleukin (IL)-12, tumor necrosis factor (TNF)-beta (= lymphotoxin-alpha) and cytolysin appeared early and before onset of clinical signs of EAE; (ii) TNF-alpha peaked at height of clinical signs of EAE; (iii) IL-10 appeared increasingly at and after clinical recovery. The early expression of IL-12 prior to the expression of interferon-gamma (IFN-gamma) mRNA shown previously is consistent with a role of IL-12 in promoting proliferation and activation of T helper 1 (Th1) type cells producing IFN-gamma. The TNF-beta mRNA expression prior to onset of clinical signs favours a role for this cytokine in disease initiation. A pathogenic effector role of TNF-alpha was suggested from these observations that TNF-alpha mRNA expression roughly paralleled the clinical signs of EAE. This may be the case also for cytolysin. IL-10-expressing cells gradually increased to high levels in the recovery phase of EAE, consistent with a function in down-regulating the CNS inflammation. From these data we conclude that there is an ordered appearance of putative disease-promoting and -limiting cytokines in the CNS during acute monophasic EAE.

M3 - Journal article

C2 - 7593556

SN - 0165-5728

VL - 61

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JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

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ER -