Literature DB >> 16106074

Interaction between the immune and central nervous systems.

John H Russell1.   

Abstract

Much of the understanding of tolerance has focused on the requirements for antigen-specific lymphocyte activation and function. However, there is increasing evidence for anatomic regulation of effector access to self antigens. Recently, a number of studies have provided evidence for tissue-specific "addressins" in chemokine/chemokine receptor pairs. The central nervous system (CNS) provides special anatomic barriers to the movement of cells from the vascular compartment to the parenchyma. Herein I raise the possibility that antigen, perhaps through specialized antigen-presenting cells, may play a role in regulating access of activated lymphocytes into the CNS parenchyma. The results suggest that a reexamination of the widely held dogma that all activated lymphocytes have access to the CNS parenchyma is necessary to understand the relationship between the immune and central nervous systems.

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Year:  2005        PMID: 16106074     DOI: 10.1385/IR:32:1-3:225

Source DB:  PubMed          Journal:  Immunol Res        ISSN: 0257-277X            Impact factor:   2.829


  24 in total

1.  Migratory activity and functional changes of green fluorescent effector cells before and during experimental autoimmune encephalomyelitis.

Authors:  A Flügel; T Berkowicz; T Ritter; M Labeur; D E Jenne; Z Li; J W Ellwart; M Willem; H Lassmann; H Wekerle
Journal:  Immunity       Date:  2001-05       Impact factor: 31.745

Review 2.  Three or more routes for leukocyte migration into the central nervous system.

Authors:  Richard M Ransohoff; Pia Kivisäkk; Grahame Kidd
Journal:  Nat Rev Immunol       Date:  2003-07       Impact factor: 53.106

3.  T-lymphocyte entry into the central nervous system.

Authors:  W F Hickey; B L Hsu; H Kimura
Journal:  J Neurosci Res       Date:  1991-02       Impact factor: 4.164

4.  Distinct roles for matrix metalloproteinase-2 and alpha4 integrin in autoimmune T cell extravasation and residency in brain parenchyma during experimental autoimmune encephalomyelitis.

Authors:  D Graesser; S Mahooti; J A Madri
Journal:  J Neuroimmunol       Date:  2000-09-22       Impact factor: 3.478

5.  Fas ligand-induced apoptosis as a mechanism of immune privilege.

Authors:  T S Griffith; T Brunner; S M Fletcher; D R Green; T A Ferguson
Journal:  Science       Date:  1995-11-17       Impact factor: 47.728

6.  The role of the antigen-presenting cell in Fas-mediated direct and bystander killing: potential in vivo function of Fas in experimental allergic encephalomyelitis.

Authors:  A R Thilenius; K A Sabelko-Downes; J H Russell
Journal:  J Immunol       Date:  1999-01-15       Impact factor: 5.422

7.  Decreased dependence of myelin basic protein-reactive T cells on CD28-mediated costimulation in multiple sclerosis patients. A marker of activated/memory T cells.

Authors:  A E Lovett-Racke; J L Trotter; J Lauber; P J Perrin; C H June; M K Racke
Journal:  J Clin Invest       Date:  1998-02-15       Impact factor: 14.808

8.  TNFR1-dependent VCAM-1 expression by astrocytes exposes the CNS to destructive inflammation.

Authors:  Mary Ann T Gimenez; Julia E Sim; John H Russell
Journal:  J Neuroimmunol       Date:  2004-06       Impact factor: 3.478

9.  Vascular cell adhesion molecule-1 modulation by tumor necrosis factor in experimental allergic encephalomyelitis.

Authors:  D M Barten; N H Ruddle
Journal:  J Neuroimmunol       Date:  1994-05       Impact factor: 3.478

Review 10.  Cell migration in the immune system: the evolving inter-related roles of adhesion molecules and proteinases.

Authors:  J A Madri; D Graesser
Journal:  Dev Immunol       Date:  2000
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