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0686 Some immunological parameters in patients with neurodegenerative diseases
Poster Abstracts
Tuesday, November 8, 2005
$273
Objective: to follow-up study the im_munological characteristics of M M F of TBE. Methods: complex examinations of 35 patients with a M M F of TBE were perfornled 1-15 years after acute period of disease. Inmlunological investigations included virus-specific antigen detection (IgM - and IgG- antibodies) by tile IF A and GABR methods Results: Antigemagglutirdnes were observed in 75-100 % of cases in reconvalescents. In the period less then 3 years after TBE in 75-100 % of cases IgG- antibodies were found in the titer of 1/400 - 1/1600, in resent years - in titer 1/100 - 1/800. We continue to reveal IgM-antibodies in the period up to 3 years after TBE in 78 % of cases. 5-7 years after the disease positive results were observed in 18,8 % of cases. Thus, steady immunological response was observed in follow-up period. Well known, that [gM-antibodies of the TBE-virus can be manifested from tile 4 t5 day in tile acute period of the disease. Tile transformation to IgG-antibodies production Call be seen on tile 21 ~t day of the disease. IgM-antibodies level goes down during the 3 month period. We consider high level of the [gM-antibodies as unfavorable sign of virus-persistence and potential chronic progredient duration of the disease. Conclusion: subjects with previous M M F o f TBE demonstrate steady inmmnological response. The long period of IgM-antibodies blood circulation confirms probability of virus persistence.
delirium. He had a 7 year history o f Hodgkin's disease treated only with mantle field radiotherapy at initial diagnosis and occasional prednisolone. He underwent splenectonly for a relapse in 2001 but refused further radio- and chemotherapy. Methods: A complete autopsy and detailed neuropathological assessment were performed. Brain tissue was examined using standard neurohistological techniques and immunocytochemical, neuronal, mxonal, astrocyfic, rnicroglial, viral and inflammatory cell markers. Results: Residual Hodgkin's lymphoma was present in the liver and abdominal lymph nodes. Neurokistological assessment of the macroscopically normal brain revealed lymphocytic perivascular cuffing, microglial nodules, eosinophilic necrotic neurones, neuronal loss and fibrous gliosis in the hippocampi and right amygdaloid nucleus. A n unusual striking feature was the presence of numerous round eosinophJlic bodies (5-50 microns) restricted to tile neuropil of the affected regions. The bodies were argyrophJlic, surrounded by a halo and positive for axonal markers. Tile bodies resembled Collins bodies ([inclusions of neuroserpin, a glycoprotein serine protease inhibitor secreted by mxons) although no neuronal intracytoplasrnic inclusion bodies ([Collins bodies) were found. Conclusion: Paraneoplastic limbic encephalitis in autopsy-proven Hodgkin's disease is associated with unusual axonal bodies.
0683 Relationship between circulating lymphocyte subset, chemokine receptor and clinical parameter in the inactive stage of relapsed remitting nmltiple sclexosis
0685 Autohmnune Inflanmlatoxy Nemopathy targeting a Myelin protein with Polymorphisul
Kinoshita, S1, Takahama, M 2, Ohnu ki, M 2, Tomioka, R 1, Nomura, K 2, Shimazu, K 1. 1Department of Neurology', Saitama Medical School,
Saitarna, Japan; 2Department of Neurology, Saitama Medical Center, Saitarna, Japan Backg*ound: We analyzed circulating lymphocyte subsets and chenlokine receptors to elucidate the inmlune response in the inactive stage of relapsed renlitting nmltiple sclerosis (RR-MS) and discussed tile mechanism of recurrence. Method: Blood samples from 45 patients with RR-MS and from 45 healthy controls were studied with flow cytometry. The relationships between chemokJne receptor and clinical parameters were compared. Results: The proportion of activated IL-2R+ T cell (CD25+) and helper-inducer cell (CD29+) of CD4 T cell increased, whereas suppressor-effector cell ( C D I l b dull+) and cytotoxic or N K cell (CDI lb bright+) of CD8 T cell decreased in the inactive stage. During the inactive stage, significantly increased proportions of CCR5, CCR3 on CD4 and/or CD8 T cells were found compared to those in control samples. No significant ratio of Thl/Th2 (CCR5/CCR3 on CD4 T cell), and Tcl/Tc2 (CCR5/CCR3 on CD8 T cell) were observed compared to those of healthy controls. A n d no relationships between the proportion of CCR5, CCR3 on T cells and clinical parameters were found in the inactive stage. Conclusion: These results suggest that the aberration of inmmne response is revealed in tile inactive stage as well as tile active stage of RR-MS. 0684 Unusual axonal bodies in autopsy-proven Hodgkin's disease-associated paraneoplastie lhnbic encephalitis Kleinig, T J 1, Thompson, PD 1, Blunlbergs, PC 2. 1Royal Adelaide
Hospital Adelaide, Australia; 2Institute of Medical and Veterinary Science, Adelaide, Australia Background: Limbic encephalitis is most commonly paraneoplastic in origin. Most cases are associated with small cell lung cancer, although many cancers have been implicated. We present tile first ([to our knowledge) autopsy-proven case of limbic encephalitis associated with Hodgkin's disease. A 39 year-old man presented with seizures and
Kondo, T 1;2, Komori, M 2, Abe, M 2, Hamasaki, M ~, Oka, N 4, Mizota, T 3, Shibuya, N ~, Matsuo, H 3. 1Departtnent of Clinical
research, Nagasaki Medical Center Of Neurology, Nagasaki, Japan; 2Department of Neurology', Fukui Redeross Hospital Fukui, Japan; 3Department of Neurology', Nagasaki Medical Center Of Neurology', Nagasaki, Japan 4Department of Rehabilitation Medicine, Minarni-kyoto National Hospital Kyoto, Japan Baekg*ound: Mutations in the Periaxin (PtLX) gene cause autosomal recessive hereditary neuropathy, but not autosomal dominant neuropathy. Although PtLX has asparagine or aspartic acid at codon 651, this polymorphism is usually non-pathogenic. However, a 27-year-old man with asparagine and asparfic acid at codon 651 of P1LX alleles and his brother suffered from Guillain-Barre Syndrome (GBS)-resembling neuropathy. Method: CD3+ T cells and CD14+ monocytes were separated from tile peripheral blood of tile above patient or control subjects. 5 x 105 of T cells rested for two days. 105 of immature dendritic cells (iDCs) differentiated from CD14+ T cells in presence of GM-CSF and IL-4. iDCs were unpulsed or pulsed with a peptide of P1LX (D651 or N651). T cells and iDCs were cocultured, and then CD69 expression on T cells was analyzed by flowcytometry after 4 hours. T cells were again treated after 10 days by unpulsed or peptide-pulsed iDC for analysis of CD69 expression. Results: CD69 expression on CD4+ T cells after coculture with N651pulsed iDCs was 1.1 tol.5% and higher than that with unpulsed iDC (0.45-0.58%) and that after coculture with D651-pulsed iDCs (0.45-1.5°,5). While CD69 expression on CD4+ T cells was less than 3°,5 after the second stimulation by unpulsed iDC, 2.9-5.1% and 9.1-12.2% of CD4+ T cells expressed CD69 after the second stimulation by D651- and N651-pulsed iDC, respectively. CD69 expression on T cells from control subjects did not differ among the three groups. Conclusion: The P R X polymorphJsm could be a target for T cellmediated autoinmmnity.
0686 SOIIle Itmnunological Parameters in Patients with Neuxodegene~afive Diseases
Tuesday, November 8, 2005
$273
Objective: to follow-up study the im_munological characteristics of M M F of TBE. Methods: complex examinations of 35 patients with a M M F of TBE were perfornled 1-15 years after acute period of disease. Inmlunological investigations included virus-specific antigen detection (IgM - and IgG- antibodies) by tile IF A and GABR methods Results: Antigemagglutirdnes were observed in 75-100 % of cases in reconvalescents. In the period less then 3 years after TBE in 75-100 % of cases IgG- antibodies were found in the titer of 1/400 - 1/1600, in resent years - in titer 1/100 - 1/800. We continue to reveal IgM-antibodies in the period up to 3 years after TBE in 78 % of cases. 5-7 years after the disease positive results were observed in 18,8 % of cases. Thus, steady immunological response was observed in follow-up period. Well known, that [gM-antibodies of the TBE-virus can be manifested from tile 4 t5 day in tile acute period of the disease. Tile transformation to IgG-antibodies production Call be seen on tile 21 ~t day of the disease. IgM-antibodies level goes down during the 3 month period. We consider high level of the [gM-antibodies as unfavorable sign of virus-persistence and potential chronic progredient duration of the disease. Conclusion: subjects with previous M M F o f TBE demonstrate steady inmmnological response. The long period of IgM-antibodies blood circulation confirms probability of virus persistence.
delirium. He had a 7 year history o f Hodgkin's disease treated only with mantle field radiotherapy at initial diagnosis and occasional prednisolone. He underwent splenectonly for a relapse in 2001 but refused further radio- and chemotherapy. Methods: A complete autopsy and detailed neuropathological assessment were performed. Brain tissue was examined using standard neurohistological techniques and immunocytochemical, neuronal, mxonal, astrocyfic, rnicroglial, viral and inflammatory cell markers. Results: Residual Hodgkin's lymphoma was present in the liver and abdominal lymph nodes. Neurokistological assessment of the macroscopically normal brain revealed lymphocytic perivascular cuffing, microglial nodules, eosinophilic necrotic neurones, neuronal loss and fibrous gliosis in the hippocampi and right amygdaloid nucleus. A n unusual striking feature was the presence of numerous round eosinophJlic bodies (5-50 microns) restricted to tile neuropil of the affected regions. The bodies were argyrophJlic, surrounded by a halo and positive for axonal markers. Tile bodies resembled Collins bodies ([inclusions of neuroserpin, a glycoprotein serine protease inhibitor secreted by mxons) although no neuronal intracytoplasrnic inclusion bodies ([Collins bodies) were found. Conclusion: Paraneoplastic limbic encephalitis in autopsy-proven Hodgkin's disease is associated with unusual axonal bodies.
0683 Relationship between circulating lymphocyte subset, chemokine receptor and clinical parameter in the inactive stage of relapsed remitting nmltiple sclexosis
0685 Autohmnune Inflanmlatoxy Nemopathy targeting a Myelin protein with Polymorphisul
Kinoshita, S1, Takahama, M 2, Ohnu ki, M 2, Tomioka, R 1, Nomura, K 2, Shimazu, K 1. 1Department of Neurology', Saitama Medical School,
Saitarna, Japan; 2Department of Neurology, Saitama Medical Center, Saitarna, Japan Backg*ound: We analyzed circulating lymphocyte subsets and chenlokine receptors to elucidate the inmlune response in the inactive stage of relapsed renlitting nmltiple sclerosis (RR-MS) and discussed tile mechanism of recurrence. Method: Blood samples from 45 patients with RR-MS and from 45 healthy controls were studied with flow cytometry. The relationships between chemokJne receptor and clinical parameters were compared. Results: The proportion of activated IL-2R+ T cell (CD25+) and helper-inducer cell (CD29+) of CD4 T cell increased, whereas suppressor-effector cell ( C D I l b dull+) and cytotoxic or N K cell (CDI lb bright+) of CD8 T cell decreased in the inactive stage. During the inactive stage, significantly increased proportions of CCR5, CCR3 on CD4 and/or CD8 T cells were found compared to those in control samples. No significant ratio of Thl/Th2 (CCR5/CCR3 on CD4 T cell), and Tcl/Tc2 (CCR5/CCR3 on CD8 T cell) were observed compared to those of healthy controls. A n d no relationships between the proportion of CCR5, CCR3 on T cells and clinical parameters were found in the inactive stage. Conclusion: These results suggest that the aberration of inmmne response is revealed in tile inactive stage as well as tile active stage of RR-MS. 0684 Unusual axonal bodies in autopsy-proven Hodgkin's disease-associated paraneoplastie lhnbic encephalitis Kleinig, T J 1, Thompson, PD 1, Blunlbergs, PC 2. 1Royal Adelaide
Hospital Adelaide, Australia; 2Institute of Medical and Veterinary Science, Adelaide, Australia Background: Limbic encephalitis is most commonly paraneoplastic in origin. Most cases are associated with small cell lung cancer, although many cancers have been implicated. We present tile first ([to our knowledge) autopsy-proven case of limbic encephalitis associated with Hodgkin's disease. A 39 year-old man presented with seizures and
Kondo, T 1;2, Komori, M 2, Abe, M 2, Hamasaki, M ~, Oka, N 4, Mizota, T 3, Shibuya, N ~, Matsuo, H 3. 1Departtnent of Clinical
research, Nagasaki Medical Center Of Neurology, Nagasaki, Japan; 2Department of Neurology', Fukui Redeross Hospital Fukui, Japan; 3Department of Neurology', Nagasaki Medical Center Of Neurology', Nagasaki, Japan 4Department of Rehabilitation Medicine, Minarni-kyoto National Hospital Kyoto, Japan Baekg*ound: Mutations in the Periaxin (PtLX) gene cause autosomal recessive hereditary neuropathy, but not autosomal dominant neuropathy. Although PtLX has asparagine or aspartic acid at codon 651, this polymorphism is usually non-pathogenic. However, a 27-year-old man with asparagine and asparfic acid at codon 651 of P1LX alleles and his brother suffered from Guillain-Barre Syndrome (GBS)-resembling neuropathy. Method: CD3+ T cells and CD14+ monocytes were separated from tile peripheral blood of tile above patient or control subjects. 5 x 105 of T cells rested for two days. 105 of immature dendritic cells (iDCs) differentiated from CD14+ T cells in presence of GM-CSF and IL-4. iDCs were unpulsed or pulsed with a peptide of P1LX (D651 or N651). T cells and iDCs were cocultured, and then CD69 expression on T cells was analyzed by flowcytometry after 4 hours. T cells were again treated after 10 days by unpulsed or peptide-pulsed iDC for analysis of CD69 expression. Results: CD69 expression on CD4+ T cells after coculture with N651pulsed iDCs was 1.1 tol.5% and higher than that with unpulsed iDC (0.45-0.58%) and that after coculture with D651-pulsed iDCs (0.45-1.5°,5). While CD69 expression on CD4+ T cells was less than 3°,5 after the second stimulation by unpulsed iDC, 2.9-5.1% and 9.1-12.2% of CD4+ T cells expressed CD69 after the second stimulation by D651- and N651-pulsed iDC, respectively. CD69 expression on T cells from control subjects did not differ among the three groups. Conclusion: The P R X polymorphJsm could be a target for T cellmediated autoinmmnity.
0686 SOIIle Itmnunological Parameters in Patients with Neuxodegene~afive Diseases