The current application is based on the hypothesis that CNS cells, including those of non-hematopoietic lineage, expressed chemokine receptors (CKRs) and thereby respond to local chemokine production. The proposal intends to define the level and cellular sources of CKR expression in the resting and inflamed CNS. It is virtually certain that infiltrating leukocytes will express the appropriate CKRs during chronic relapsing EAE. It remains unknown whether CKR expression on endogenous neural cells is upregulated during inflammation. The hypothesis will be addressed with three specific aims: (1) analysis of steady state levels of CKR, mRNA expression in the resting CNS and during Ch-R EAE; (2) identification of cells that express CKRs within the resting CNS and during Ch-R EAE; (3) analysis of CKR expression following stereotactic injection of TNF-a injection.
| Ransohoff, Richard M (2009) Chemokines and chemokine receptors: standing at the crossroads of immunobiology and neurobiology. Immunity 31:711-21 |
| Glabinski, Andrzej R; Bielecki, Bartosz; Kolodziejski, Pawel et al. (2003) TNF-alpha microinjection upregulates chemokines and chemokine receptors in the central nervous system without inducing leukocyte infiltration. J Interferon Cytokine Res 23:457-66 |
| Glabinski, Andrzej R; Bielecki, Bartosz; O'Bryant, Sage et al. (2002) Experimental autoimmune encephalomyelitis: CC chemokine receptor expression by trafficking cells. J Autoimmun 19:175-81 |
| Glabinski, A R; O'Bryant, S; Selmaj, K et al. (2000) CXC chemokine receptors expression during chronic relapsing experimental autoimmune encephalomyelitis. Ann N Y Acad Sci 917:135-44 |
| Glabinski, A R; Krakowski, M; Han, Y et al. (1999) Chemokine expression in GKO mice (lacking interferon-gamma) with experimental autoimmune encephalomyelitis. J Neurovirol 5:95-101 |
