The possible involvement of sema3A and sema4A in the pathogenesis of multiple sclerosis
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作者:
Eiza, N.
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Bnai Zion Med Ctr, Prote Unit, Haifa, Israel
Technion Israel Inst Technol, Rappaport Fac Med, Haifa, IsraelBnai Zion Med Ctr, Prote Unit, Haifa, Israel
Eiza, N.
[1
,4
]
Garty, M.
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机构:
Bnai Zion Med Ctr, Neurol Dept, Haifa, IsraelBnai Zion Med Ctr, Prote Unit, Haifa, Israel
Garty, M.
[2
]
Staun-Ram, E.
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机构:
Carmel Hosp, Multiple Sclerosis Ctr, Haifa, Israel
Technion Israel Inst Technol, Rappaport Fac Med, Haifa, Israel
Carmel Hosp, Neuroimmunol Unit, Haifa, IsraelBnai Zion Med Ctr, Prote Unit, Haifa, Israel
Staun-Ram, E.
[3
,4
,5
]
Miller, A.
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机构:
Carmel Hosp, Multiple Sclerosis Ctr, Haifa, Israel
Technion Israel Inst Technol, Rappaport Fac Med, Haifa, Israel
Carmel Hosp, Neuroimmunol Unit, Haifa, IsraelBnai Zion Med Ctr, Prote Unit, Haifa, Israel
Miller, A.
[3
,4
,5
]
Vadasz, Z.
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Bnai Zion Med Ctr, Prote Unit, Haifa, Israel
Technion Israel Inst Technol, Rappaport Fac Med, Haifa, IsraelBnai Zion Med Ctr, Prote Unit, Haifa, Israel
Vadasz, Z.
[1
,4
]
机构:
[1] Bnai Zion Med Ctr, Prote Unit, Haifa, Israel
[2] Bnai Zion Med Ctr, Neurol Dept, Haifa, Israel
[3] Carmel Hosp, Multiple Sclerosis Ctr, Haifa, Israel
[4] Technion Israel Inst Technol, Rappaport Fac Med, Haifa, Israel
Background: Immune semaphorins are widely accepted to have functional impact on autoimmune diseases. Objectives: To assess the status of sema3A and sema4A in the pathogenesis of Multiple Sclerosis (MS). Results: Sema3A expression on (T regulatory cells)Tregs was decreased in MS patients, compared to healthy controls (35.85 +/- 16.7% vs 88.27 +/- 3.8%; p <= 0.001). Serum levels of sema3A were decreased in MS patients 2.95 +/- 0.43 vs 18.67 +/- 5.7 ng/ml in healthy individuals; p <= 0.001. Sema4A serum levels were increased in MS patients compared to healthy individuals (12.99 +/- 8.6 vs 5.83 +/- 3.91 ng/ml; p <= 0.001). Sema3A and sema4A serum levels were found to be in negative/positive correlation with MS disease severity (r(s) = 0.62, r(s) =-0.49, respectively). Conclusion: We show that sema3A is a regulatory molecule in MS, whereas sema4A is a stimulatory one. Targeting sema3A and sema4A could become a potential therapeutic approach in MS.