title: Increased lymphocyte beta-adrenergic receptor density in progressive multiple sclerosis is specific for the CD8+, CD28- suppressor cell.
abstract: Beta-adrenergic receptor density on T cells from healthy humans is greatest on suppressor cells (CD8+, CD28-) and the effect of catecholamines, secreted by the sympathetic nervous system, predominates on this subset. The sympathetic skin response, a measure of sympathetic nervous system function, is absent in most patients with chronic progressive multiple sclerosis (MS). We measured beta-adrenergic receptor density on suppressor cells, cytotoxic cells, and monocytes from patients with chronic progressive MS and healthy control subjects. Control receptor density on suppressor cells was 2.8 +/- 0.3 fmol/10(6) cells versus a density of 5.1 +/- 0.7 fmol/10(6) cells for patients. Cytotoxic cell (CD8+, CD28+) receptor density was 1.4 +/- 0.4 fmol/10(6) cells in control subjects and 0.9 +/- 0.3 fmol/10(6) cells in the patients. Monocytes displayed beta-adrenergic receptor densities of 2.6 +/- 0.4 fmol/10(6) cells in normal individuals and 2.7 +/- 0.4 fmol/10(6) cells in the patient group. CD8 lymphocyte beta-adrenergic receptor densities in patients with relapsing-remitting and those with stable MS were not different from control values, yet were significantly less than the values for patients with chronic progressive MS. We find that mononuclear cells from healthy control subjects and patients with chronic progressive MS proliferate in response to 200 units/ml of recombinant human interleukin-2 (IL-2) similarly. However, IL-2 treatment increased beta-adrenergic receptor density on normal mononuclear cells, but failed to increase it on mononuclear cells from patients with chronic progressive MS.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Neurology, University of Chicago, IL.
authors.forename: J W
authors.initials: JW
authors.lastname: Karaszewski
authors.forename: A T
authors.initials: AT
authors.lastname: Reder
authors.forename: B
authors.initials: B
authors.lastname: Anlar
authors.forename: W C
authors.initials: WC
authors.lastname: Kim
authors.forename: B G
authors.initials: BG
authors.lastname: Arnason
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000032:analysis*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis*; D001327:Autoimmune Diseases / Q000276:immunology / Q000473:pathology*; D018106:CD28 Antigens; D016827:CD8 Antigens / Q000032:analysis*; D002478:Cells, Cultured; D006801:Humans; D007376:Interleukin-2 / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000187:drug effects; D008875:Middle Aged; D008954:Models, Biological; D009103:Multiple Sclerosis / Q000276:immunology / Q000473:pathology*; D009475:Neurons, Afferent / Q000378:metabolism / Q000473:pathology; D010869:Pindolol / Q000031:analogs & derivatives / Q000494:pharmacology; D011943:Receptors, Adrenergic, beta / Q000032:analysis* / Q000187:drug effects; D011994:Recombinant Proteins / Q000494:pharmacology; D016176:T-Lymphocyte Subsets / Q000737:chemistry* / Q000276:immunology / Q000473:pathology; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D018106:CD28 Antigens; D016827:CD8 Antigens; D007376:Interleukin-2; D011943:Receptors, Adrenergic, beta; D011994:Recombinant Proteins; C047975:cyanopindolol; D010869:Pindolol