Th1 dominance in HAM/TSP and the optico-spinal form of multiple sclerosis versus Th2 dominance in mite antigen-specific IgE myelitis

Clinical and laboratory characteristics of atopic myelitis: Korean experience

“…In addition, NMO-IgG, which is frequently present in NMO or OSMS [11], was detected in none of the AM patients, suggesting that AM is a different entity from NMO. Immunologically, AM appears to be different from other myelitis diseases associated with MS or HTLV-1-associated myelopathy/tropical spastic paraparesis in that type 2 helper T (Th2) cell response is predominant in the former whereas Th1 cell response is predominant in the latter [21][22][23]. More recently, CSF cytokine/chemokine analysis showing upregulation of chemokine-ligand-11/interleukin-9, which is important for eosinophil recruitment and maturation, has lent further supported the allergic nature of AM [24].…”

Time-dependent cytokine deviation toward the Th2 side in Japanese multiple sclerosis patients with interferon beta-1b

“…Moreover, in some studies, marked Th1 and Tc1 shifts are present in the peripheral blood throughout relapse and remission phases in OS-MS while a Th1 shift was only evident in the relapse phase in C-MS [15,35,36]. However, in the present study, a reduction in the IFN-g/IL-4 ratio during IFNh therapy was commonly seen in both OS-MS and C-MS, suggesting that a common mechanism may be partly operative in the two MS subtypes, and that the reduction in the intracellular IFNg/IL-4 ratio by IFNh may exert beneficial effects on this process.…”

Increased mRNA Expression of Th1-Cytokine Signaling Molecules in Patients with HTLV-I-Associated Myelopathy/Tropical Spastic Paraparesis

“…Previously, cytokine studies in HAM/TSP patients have revealed elevated serum, cerebrospinal fluid (CSF) and CD4 + cell culture supernatant levels of interferon-γ (IFN-γ ) (Kuroda and Matsui 1993;Nishiura et al 1996;Furuya et al 1999) and high intracellular IFN-γ + /interleukin-4 + (IL-4 + ) cell ratio in CD4 + T cells (Horiuchi et al 2000), suggesting that the immunological state of HAM/TSP patients is under Th1 activation (Nakamura et al 2000b). On the other hand, HTLV-I infection also causes production of Th2 cytokines (Mogensen and Paludan 2001).…”