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Nöro-Behçetli hastaların beyin omirilik sıvısında mikobakteriyel ısı şoku proteinine karşı antikor yanıtı

Humoral immune response againts 65kD heat shock protein in the cerebrospinal fluid of neuro-Behcet patients

  1. Tez No: 60108
  2. Yazar: BANU TAŞÇI
  3. Danışmanlar: DOÇ. DR. PİRAYE SERDAROĞLU
  4. Tez Türü: Tıpta Uzmanlık
  5. Konular: Nöroloji, Neurology
  6. Anahtar Kelimeler: Behçet hastalığı, Serebrospinal sıvı, Sıcaklık şoku proteinleri, Behcet syndrome, Cerebrospinal fluid, Heat shock proteins
  7. Yıl: 1997
  8. Dil: Türkçe
  9. Üniversite: İstanbul Üniversitesi
  10. Enstitü: Tıp Fakültesi
  11. Ana Bilim Dalı: Nöroloji Ana Bilim Dalı
  12. Bilim Dalı: Belirtilmemiş.
  13. Sayfa Sayısı: Belirtilmemiş.

Özet

Özet yok.

Özet (Çeviri)

Summary. Although systemic immune reactivity to 65 kD mycobacterial heat shock protein (m-HSP65) has been shown previously in Behcet's disease (BD), local immune response was not investigated. We studied anti m-HSP65 IgG, IgM and IgA antibodies in the serum and cerebrospinal fluid (CSF) of 40 BD patients (25 with cerebral parenchymal involvement (p- NBD), 7 with intracranial hypertension (ih-NBD), 8 without CNS involvement), 30 with multiple sclerosis (MS) and 24 with non-inflammatory CNS disorders (NIC). Significantly higher CSF IgG responses were detected in p-NBD patients (ELISA ratio: 1.3±0.9) compared to NIC (0.7±0.4, p<0.01). In p-NBD patients IgG, IgM or IgA CSF anti m-HSP65 positivity rate was 48% (12/25), being significantly higher when compared to MS (3/30; p< 0.03) and NIC (3/24; p<0.01). CSF anti m-HSP65 IgG ratios was found to correlate with the duration of BD (r=0.4, p<0.04), but not with the duration of neurological involvement. The serum antibody levels were elevatedin ih-NBD patients. There was no positive CSF response in the same group. These findings are in accordance with the previous clinical studies, suggesting different types of involvement in ih-NBD, other than p-NBD. In multiple sclerosis patients, responses did not differ significantly from NIC, which implicates a spesific role of high levels of anti m-hsp65 antibodies in the pathogenesis of p-NBD. The oligodendrocyte damage, glial reactions and perivenular infiltration in p-NBD might be due to increased levels of y8 T cells passing through a damaged blood brain barrier, if one should take account of the findings of the immunohistological studies in MS. These results implicate an increased local humoral response to m-HSP65 in the CSF of p-NBD patients which might be related to the pathogenesis of neurological involvement. 33

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