Cytokines

  1. Cytokines regulate T-Cell activation in Multiple Sclerosis
    Ann Neurol 43: 340-9 (1998)

  1. Cytokine mRNA expression in patients with Multiple Sclerosis and Fatigue
    Mult Scler 2004 Apr;10(2):165-9

  2. Fatigue in Multiple Sclerosis: an example of Cytokine mediated sickness behaviour?
    J Neurol NeuroSurg Psychiatry 2006 Jan;77(1):34-9

  3. ProteoLipid Protein (PLP) implicated in Multiple Sclerosis
    Journal of NeuroImmunology 84(2), 172-178

  4. Transforming Growth Factor (TGF)-beta1, -beta2, and -beta3 and TGF-beta type I & type II in Multiple Sclerosis lesions
    J NeuroPathol Exp Neurol 1999 Feb;58(2):174-87

  5. CCR5+ & CXCR3+ T-Cells are increased in Multiple Sclerosis
    The National Academy of Sciences 0027-8424/99/966873-6
    Vol. 96, Issue 12, 6873-6878, June 8, 1999

  6. MCP-1, MCP-2 & MCP-3 expression in Multiple Sclerosis lesions
    J NeuroImmunol 1998 Jun 1;86(1):20-9

  7. Mast Cells stimulate Immune response against bacteria
    PNAS, Vol. 96, Issue 14, 8110-8115, July 6, 1999

  8. alpha B-crystallin, a candidate AutoAntigen in Multiple Sclerosis
    J Immunol 162: 129-35 (1999)

  9. AutoAntiBodies associated with Myelin damage In MS
    Nat Med 1999 Feb;5(2):170-5

  10. Cytokine profile of Myelin Basic Protein reactive T-Cell in MS
    AutoImmunity 28: 77-89 (1998)

  11. Interferon-ß decreased Tumor Necrosis Factor binding in MS
    Arch Neurol Jan. 1999;56:71-78

  12. CD4+ & CD8+ T-Cells make discrete contributions to DeMyelination and Neurologic Disease in a Viral model of Multiple Sclerosis
    J Virol 1998 Sep;72(9):7320-9

  13. Initiation and regulation of CNS AutoImmunity
    Crit Rev Immunol 1997; 17(5-6): 469-480

  14. Tumor Necrosis Factor may limit severe CNS pathology
    Nat Med 1998 Jan;4(1):78-83

  15. Tumor Necrosis Factor alpha precedes Multiple Sclerosis activity
    Arch Neurol June 1998;55:793-798

  16. Proinflammatory Cytokines & Tumor Necrosis Factor
    Brain 119 ( Pt 1): 213-23 (1996)

#1

Cytokines Regulate T-Cell
Activation In MS

Martino G; Grohovaz F; Brambilla E; Codazzi F; Consiglio A; Clementi E; Filippi M; Comi G; Grimaldi LM
Ann Neurol 43: 340-9 (1998)
San Raffaele Scientific Institute, DIBIT, Dept of Neurology, Univ of Milano, Italy
UI# 98165376
Abstract

Central Nervous System (CNS) lesions typical of Multiple Sclerosis (MS) are characterized by DeMyelinating inflammatory infiltrates that contain few CNS Antigen-Specific AutoReactive T-Cells and a multitude of Pathogenic Non-Antigen-Specific MonoNuclear Cells.

Here, we report that in patients with MS the combined action of Interferon-gamma (IFN-γ), Tumor Necrosis Factor-alpha (TNFalpha), InterLeukin IL-2, and IL-6 leads to the activation of most peripheral T-Cells.

Mainly CD4 Memory Cells, by promoting a persistent IntraCellular Calcium increase via two independent signaling pathways.

The activation of these pathways, one activated by IFN-γ and the other by the combination TNFalpha/IL-2/IL-6, is independent from Myelin Antigens.

And precedes by 2 weeks, phases of disease activity (eg, clinical relapses and/or appearance of Gadolinium enhancing lesions on Brain Magnetic Resonance Imaging scans during 1 year of follow-up).

Our results indicate that an appropriate combination of the four Cytokines, three with a ProInflammatory profile and one necessary for T-Cell growth and differentiation, can activate in an Antigen-Independent fashion most peripheral T-Cells from MS patients.

This mechanism is likely to contribute to the recruitment of NonSpecific Lymphocytes into the cellular activation processes leading to CNS DeMyelination and may represent a major target for Immune intervention in MS.

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