title: Severe T-cell depletion from the PALS leads to altered spleen composition in common marmosets with experimental autoimmune encephalomyelitis (EAE).
abstract: Recent data suggest that the spleen is a crucial component of the immune system in the development of experimental autoimmune encephalomyelitis (EAE) in marmoset monkeys. Using immunohistochemistry, we investigated changes in the distribution of leukocytes in the spleen associated with clinical symptoms of EAE. Animals without EAE displayed well-developed T- and B-cell areas, germinal centers and red pulp. In contrast, a marked depletion of periarteriolar T cells with preservation of other elements was found in animals with clinical EAE. These findings suggest that immune responses within the spleen are impaired during a paralysing inflammatory process in the central nervous system.
authors.affiliation: Department of Immunology, Erasmus MC, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands.
authors.forename: Alex F
authors.initials: AF
authors.lastname: De Vos
authors.forename: Debby A J
authors.initials: DA
authors.lastname: van Riel
authors.forename: Marjan
authors.initials: M
authors.lastname: van Meurs
authors.forename: Herbert P M
authors.initials: HP
authors.lastname: Brok
authors.forename: Louis
authors.initials: L
authors.lastname: Boon
authors.forename: Rogier Q
authors.initials: RQ
authors.lastname: Hintzen
authors.forename: Eric
authors.initials: E
authors.lastname: Claassen
authors.forename: Bert A
authors.initials: BA
authors.lastname: 't Hart
authors.forename: Jon D
authors.initials: JD
authors.lastname: Laman
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D015703:Antigens, CD / Q000145:classification / Q000378:metabolism; D002144:Callithrix; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism; D007075:Immunoglobulin M / Q000378:metabolism; D007150:Immunohistochemistry / Q000379:methods; D008213:Lymphocyte Activation / Q000187:drug effects / Q000502:physiology; D008212:Lymphocyte Depletion; D008214:Lymphocytes / Q000145:classification / Q000378:metabolism* / Q000473:pathology / Q000648:ultrastructure; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism; D046529:Microscopy, Electron, Transmission / Q000379:methods; D009186:Myelin Sheath; D009687:Nuclear Proteins / Q000378:metabolism; D010950:Plasma Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D011971:Receptors, Immunologic / Q000378:metabolism; D063267:Sialic Acid Binding Ig-like Lectin 1; D013154:Spleen / Q000378:metabolism* / Q000473:pathology / Q000648:ultrastructure; D013601:T-Lymphocytes / Q000276:immunology* / Q000648:ultrastructure / Q000821:virology; D020931:ran GTP-Binding Protein / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D008562:Membrane Glycoproteins; D009687:Nuclear Proteins; D011971:Receptors, Immunologic; C571166:SIGLEC1 protein, human; D063267:Sialic Acid Binding Ig-like Lectin 1; D000135:Acid Phosphatase; D020931:ran GTP-Binding Protein