Table 11.2.

Mediators associated with experimental autoimmune encephalomyelitis

	Nature of associationa
Cytokines	Active disease/relapse (reference*)		Remission/suppression (reference*)	Disease modulated by antibody or inhibitors (reference)*
IL-1	+	*1	−	Yes	*22
IL-2	+	2,3	−	NRb
IL-3	+	4	−	NR
IL-4	−	+	−
IL-6	+	1	−	NR
IL-10	−	+	*1,5
IL-12	+	5	−	Yes	12
IL-13	−	+	13
IL-18	+	6	−	Yes	14
IFN-γ	+	1,3	+c	Yesd	3,15
TNF-α	+	1,5,7	−	Yes	16
LT-α	+	8	−	Yes	8
TGF-β	−	+	17,18
IFN-α	?	+	19 (directly inhibited EAE)
Chemokinesd
MCP-1	+	9	−	Yes	20,21
MIP-1α	+	9,10	−	Yes	10,20,21
MIP-1β	+	9	−	NR
RANTES	+	9	−	No	20,21
IP-10	+	9	−	Yes	20
C10	+	11	−	NR
MIP-2	−	−	10,20
TCA-3	+e	9

References: 1 = Okuda et al (1995); 2 = Litzenburger et al (1998); 3 = Owens et al (1994); 4 = Campbell et al (1998); 5 = Issazadeh et al (1995); 6 = Jander and Stoll (1998); 8 = Hjelstrom et al (1998); 9 = Stalder et al (1998); 10 = Karpus (1995); 11 = Bruce et al (1996); 12 = Leonard et al (1995); 13 = Cash et al (1994); 14 = Wildbaum et al (1998); 15 = Popko et al (1997); 16 = Selmaj and Raine (1995); 17 = Johns and Sriram (1993); 18 = Racke et al (1991); 19 = Billian et al (1988); 20 = Ransohoff (1999); 21 = Youssef et al (1998); 22 = Martin and Near (1995).

^aReferences cited are as far as possible those that identified the mediators in question in the CNS, at or near sites of pathology, or reviews that summarize those data.

^bNR: No reports.

^cThe viewpoint that IFN-γ suppresses experimental allergic encephalomyelitis is not consistent with recent data, but was a logical interpretation of antibody and knockout experiments in their time.

^dThe literature on this topic is broad, so only a few reviews have been cited.

^eAssociation in this case was on the basis of expression by encephalitogenic T cells.

Reproduced fromT. Owens et al (2001).

© 2006