@article {542636,
	title = {Recovery from EAE is associated with decreased survival of encephalitogenic T cells in the CNS of B7-1/B7-2-deficient mice.},
	journal = {Eur J Immunol},
	volume = {33},
	number = {7},
	year = {2003},
	month = {2003 Jul},
	pages = {2022-2032},
	abstract = {Adoptive transfer experiments using C57BL/6 mice lacking B7-1 and B7-2 as recipients of wt (wt) encephalitogenic T cells demonstrate a key role for B7 costimulation during the effector phase of experimental autoimmune encephalomyelitis (EAE). Following transfer of encephalitogenic T cells, B7-1/B7-2-deficient (-/-) recipients develop a transient and mild disease as compared to wt recipients. To understand the mechanism by which B7-1/B7-2 may influence the effector phase of EAE, we analyzed T cells, pro-inflammatory cytokines and chemokines within the CNS of wt and B7-1/B7-2-/- recipients at different times after adoptive transfer of activated myelin specific T cells. There was a marked decline in T cells and inflammatory mediators in the CNS of B7-1/B7-2-/- recipients by day 30 post transfer. B7-1/B7-2-/- mice developed more TUNEL+ apoptotic cells in the parenchyma and greater ratios of TUNEL+ cells/parenchymal foci than wt mice resulting in virtual disappearance of parenchymal foci. Therefore, without B7-1 and B7-2 costimulation in the target organ, there is increased T cell apoptosis and attenuation of inflammation. These results indicate that B7-1 and B7-2 provide critical costimulatory signals for sustaining survival of pathogenic T cells within the central nervous system parenchyma during the effector phase of EAE and suggest novel treatment approaches in the effector phase of autoimmune diseases.},
	keywords = {Animals, Antigens, CD, Antigens, CD80, Antigens, CD86, Apoptosis, Cell Survival, Central Nervous System, Encephalomyelitis, Autoimmune, Experimental, Membrane Glycoproteins, Mice, T-Lymphocytes},
	issn = {0014-2980},
	doi = {10.1002/eji.200323180},
	author = {Chang, Tammy T and Sobel, Raymond A and Wei, Tao and Ransohoff, Richard M and Kuchroo, Vijay K and Sharpe, Arlene H}
}
