PMID- 20420170
OWN - NLM
STAT- MEDLINE
DCOM- 20100617
LR  - 20151119
IS  - 1881-6096 (Print)
IS  - 1881-6096 (Linking)
VI  - 62
IP  - 4
DP  - 2010 Apr
TI  - [Pathogenesis of paraneoplastic neurological syndromes].
PG  - 309-18
AB  - Paraneoplastic neurological syndromes (PNS) are thought to be caused by 
      autoimmune processes triggered by the cancer and directed against antigens common 
      to both the cancer and the nervous system. There are several clinical phenotypes 
      in combinations with the neurological syndromes, origin of cancer and the 
      specific autoantibodies. PNS with antibodies against channel receptors on the 
      cell surface tend to respond favorably to antibody-depletion therapies; this 
      suggests that the antibodies detected in these PNS groups are closely related to 
      their pathogenesis. PNS having the antibodies against intracellular proteins 
      might be caused by cytotoxic T cell-mediated cell death. This is because the 
      following findings; 1) the prominent mononuclear cells in CSF, 2) the 
      infiltration of inflammatory cells, mainly CD8+ T lymphocytes, in the tumor and 
      the nervous tissue. In addition, T cell receptor usage of infiltrated T 
      lymphocytes in the affected CNS lesions has been shown to be oligoclonal. We 
      observed that the disease model could not be produced using only 
      anti-intracellular antibodies such as anti-Yo or anti-Hu antibodies, but that CTL 
      activity could be induced in CD8+ T cells isolated from the peripheral 
      mononuclear cells obtained from PNS patients with anti-Yo or anti-Hu antibodies. 
      The anti-Yo- or anti-Hu-antibody-positive patients possess common human leukocyte 
      antigen (HLA) class I motifs. This implies that in patients with anti-Yo or 
      anti-Hu antibodies, the presentation of the certain antigen peptides on the cell 
      surface could be used to stimulate CD8+ T lymphocytes that could attack their 
      target tissues as effectors. Antigen-specific CTL-mediated cell death has been 
      observed in cancer immunology and PNS appears to be a potential candidates for a 
      future CTL-mediated neurological disease model.
FAU - Tanaka, Keiko
AU  - Tanaka K
AD  - Department of Neurology, Kanazawa Medical University, 1-1 Uchinada, Kahoku-gun, 
      Ishikawa 920-0293, Japan.
LA  - jpn
PT  - English Abstract
PT  - Journal Article
PT  - Review
PL  - Japan
TA  - Brain Nerve
JT  - Brain and nerve = Shinkei kenkyu no shinpo
JID - 101299709
RN  - 0 (Autoantibodies)
RN  - 0 (CDR2 protein, human)
RN  - 0 (ELAV Proteins)
RN  - 0 (Nerve Tissue Proteins)
SB  - IM
MH  - Autoantibodies
MH  - *Autoimmunity
MH  - CD8-Positive T-Lymphocytes/immunology
MH  - Cell Death
MH  - ELAV Proteins
MH  - Humans
MH  - Immunotherapy
MH  - Neoplasms/immunology/pathology
MH  - Nerve Tissue Proteins/immunology
MH  - Nervous System/immunology
MH  - Paraneoplastic Syndromes, Nervous System/*immunology/therapy
MH  - T-Lymphocytes, Cytotoxic/immunology
RF  - 63
EDAT- 2010/04/28 06:00
MHDA- 2010/06/18 06:00
CRDT- 2010/04/28 06:00
PHST- 2010/04/28 06:00 [entrez]
PHST- 2010/04/28 06:00 [pubmed]
PHST- 2010/06/18 06:00 [medline]
PST - ppublish
SO  - Brain Nerve. 2010 Apr;62(4):309-18.