Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1991-11-7
pubmed:abstractText
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)
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0364-5134
pubmed:author
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
42-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:1656847-Adult, pubmed-meshheading:1656847-Antigens, CD, pubmed-meshheading:1656847-Antigens, CD28, pubmed-meshheading:1656847-Antigens, CD8, pubmed-meshheading:1656847-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:1656847-Autoimmune Diseases, pubmed-meshheading:1656847-Cells, Cultured, pubmed-meshheading:1656847-Humans, pubmed-meshheading:1656847-Interleukin-2, pubmed-meshheading:1656847-Lymphocyte Activation, pubmed-meshheading:1656847-Middle Aged, pubmed-meshheading:1656847-Models, Biological, pubmed-meshheading:1656847-Multiple Sclerosis, pubmed-meshheading:1656847-Neurons, Afferent, pubmed-meshheading:1656847-Pindolol, pubmed-meshheading:1656847-Receptors, Adrenergic, beta, pubmed-meshheading:1656847-Recombinant Proteins, pubmed-meshheading:1656847-T-Lymphocyte Subsets, pubmed-meshheading:1656847-Up-Regulation
pubmed:year
1991
pubmed:articleTitle
Increased lymphocyte beta-adrenergic receptor density in progressive multiple sclerosis is specific for the CD8+, CD28- suppressor cell.
pubmed:affiliation
Department of Neurology, University of Chicago, IL.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't