PMID- 20345941
OWN - NLM
STAT- MEDLINE
DCOM- 20101015
LR  - 20220311
IS  - 1528-1167 (Electronic)
IS  - 0013-9580 (Linking)
VI  - 51
IP  - 9
DP  - 2010 Sep
TI  - Evaluation of the innate and adaptive immunity in type I and type II focal 
      cortical dysplasias.
PG  - 1763-73
LID - 10.1111/j.1528-1167.2010.02547.x [doi]
AB  - PURPOSE: Induction of inflammatory pathways has been reported in epileptic 
      patients with focal malformations of cortical development. In the present study 
      we examined the innate and adaptive immune responses in focal cortical dysplasia 
      (FCD) with different histopathologic and pathogenetic features. METHODS: The 
      inflammatory cell components and the induction of major proinflammatory pathways 
      and molecules [complement pathway, interleukin (IL)-1beta, and chemokine monocyte 
      chemotactic protein-1 (MCP1)] was investigated in surgical specimens of sporadic 
      type IA and type IIB FCD using immunocytochemical methods. RESULTS: FCD II but 
      not FCD I cases exhibit activation of the mammalian target of rapamycin (mTOR) 
      cascade with strong neuronal expression of the phosphorylated isoform of S6 
      protein. Microglia reactivity was increased in all lesions (FCD I and II) 
      compared to control tissue; however, the number of HLA-DR-positive cells was 
      significantly higher in FCD II than in FCD I. In FCD II specimens we also 
      observed perivascular and parenchymal T lymphocytes (CD3(+) ), with a 
      predominance of CD8(+) T-cytotoxic/suppressor lymphocytes, as well as a few 
      dendritic cells. Expression of components of the complement cascade, IL-1beta, and 
      MCP1 was prominent in FCD II cases. DISCUSSION: Our findings indicate a prominent 
      activation of both innate and adaptive immunity, with involvement of different 
      inflammatory pathways in FCD II cases, supporting the possible involvement of 
      inflammation in the epileptogenesis of these lesions, as well as the notion that 
      FCD II is pathologically distinct from FCD I.
CI  - Wiley Periodicals, Inc. (c) 2010 International League Against Epilepsy.
FAU - Iyer, Anand
AU  - Iyer A
AD  - Department of (Neuro) Pathology, Academic Medical Center, University of 
      Amsterdam, Amsterdam, The Netherlands.
FAU - Zurolo, Emanuele
AU  - Zurolo E
FAU - Spliet, Wim G M
AU  - Spliet WG
FAU - van Rijen, Peter C
AU  - van Rijen PC
FAU - Baayen, Johannes C
AU  - Baayen JC
FAU - Gorter, Jan A
AU  - Gorter JA
FAU - Aronica, Eleonora
AU  - Aronica E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Epilepsia
JT  - Epilepsia
JID - 2983306R
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1)
RN  - 0 (Receptors, Metabotropic Glutamate)
SB  - IM
MH  - Adaptive Immunity/immunology/*physiology
MH  - Cerebral Cortex/immunology/pathology
MH  - Chemokine CCL2/genetics/immunology
MH  - Complement Activation/genetics/immunology
MH  - Dendritic Cells/immunology/pathology
MH  - Epilepsy/genetics/*immunology/pathology
MH  - Humans
MH  - Immunity, Innate/genetics/immunology/*physiology
MH  - Immunohistochemistry
MH  - Inflammation/genetics/immunology/pathology
MH  - Interleukin-1/genetics/immunology
MH  - Malformations of Cortical Development/genetics/*immunology/pathology
MH  - Microglia/immunology/pathology
MH  - Neurons/immunology/pathology/physiology
MH  - Receptors, Metabotropic Glutamate/genetics/immunology
EDAT- 2010/03/30 06:00
MHDA- 2010/10/16 06:00
CRDT- 2010/03/30 06:00
PHST- 2010/03/30 06:00 [entrez]
PHST- 2010/03/30 06:00 [pubmed]
PHST- 2010/10/16 06:00 [medline]
AID - EPI2547 [pii]
AID - 10.1111/j.1528-1167.2010.02547.x [doi]
PST - ppublish
SO  - Epilepsia. 2010 Sep;51(9):1763-73. doi: 10.1111/j.1528-1167.2010.02547.x.