Elevated expression of MCP-1, IL-2 and PTPR-N in basal ganglia of Tourette syndrome cases.
BACKGROUND
Post-infectious autoimmunity has been implicated in pathogenesis of Tourette's syndrome (TS) but no evidence of inflammation in central nervous system has been reported yet. We evaluated the expression of genes encoding selected inflammatory factors in post-mortem specimen of adult TS patients: interferon-γ (a cytokine released from CD8 and Thelper 1 CD4 subset of T lymphocytes), interleukin-2 (IL-2, a growth factor derived from T lymphocytes), interleukin-1 β (a cytokine involved in initiation of inflammation), monocyte chemotactic factor -1 (MCP-1, a marker of chronic inflammation) and CD45 (pan-leukocytic marker). For validation purposes, we determined expression of three genes that were previously reported to be elevated in post-mortem specimen of other TS cases: protein tyrosine phosphatase receptor-N (PTPR-N), PTPR-U and recoverin.


METHODS
Total RNA was isolated from formalin fixed brain tissue sections of basal ganglia area from four patients with TS and four control subjects, and real-time reverse transcription-polymerase chain reaction analysis was employed to quantitatively evaluate gene expression of the selected genes.


RESULTS
Significantly increased expression of MCP-1, IL-2 and PTPR-N was observed in TS cases (6.5-fold, 2.3-fold and 16.1-fold increase, respectively, p<0.05).


CONCLUSIONS
Elevated expression of MCP-1 and IL-2 supports the possibility of chronic inflammatory processes in the basal ganglia. Replication of elevated expression of PTPR-N in TS specimen suggests that pathway(s) involving this molecule may be important in TS pathogenesis.
Morer
Astrid
A
Department of Immunobiology, Child Study Center of Yale University School of Medicine, New Haven, CT, USA.
Chae
Wookjin
W
Henegariu
Octavian
O
Bothwell
Alfred L M
AL
Leckman
James F
JF
Kawikova
Ivana
I
D000328:Adult; D000368:Aged; D001344:Autopsy; D001479:Basal Ganglia / Q000276:immunology* / Q000378:metabolism; D018932:Chemokine CCL2 / Q000235:genetics / Q000276:immunology*; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology; D053583:Interleukin-1beta / Q000235:genetics / Q000276:immunology; D007376:Interleukin-2 / Q000235:genetics / Q000276:immunology*; D017493:Leukocyte Common Antigens / Q000235:genetics / Q000276:immunology; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012313:RNA; D054623:Receptor-Like Protein Tyrosine Phosphatases, Class 2 / Q000235:genetics / Q000276:immunology; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8 / Q000235:genetics / Q000276:immunology*; D051603:Recoverin / Q000235:genetics / Q000276:immunology; D005879:Tourette Syndrome / Q000235:genetics / Q000276:immunology*
C111835:CCL2 protein, human; D018932:Chemokine CCL2; D053583:Interleukin-1beta; D007376:Interleukin-2; D051603:Recoverin; D012313:RNA; D007371:Interferon-gamma; D017493:Leukocyte Common Antigens; C516769:PTPRC protein, human; C516862:PTPRN protein, human; C516868:PTPRU protein, human; D054623:Receptor-Like Protein Tyrosine Phosphatases, Class 2; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8