Linked Life Data

11051279

Source:http://linkedlifedata.com/resource/pubmed/id/11051279

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-1-26
pubmed:abstractText
To investigate the pathophysiology of chronic urticaria (CU) in light of the abundant evidences that it is an autoimmune disease and to define some cellular markers in B/T lymphocytes that could be of pathogenic significance, we investigated 14 patients suffering from CU, compared to 7 contact dermatitis patients and 10 normal control individuals. We tested the expression of CD5, B7.1 (CD80), CD23, and CD25 on B cells and of CD(40L)) and CD25 on T cells from all studied individuals. We also tested B cell proliferation upon their activation followed by dexamethazone induced inhibition of proliferation. The expression of bcl-2 protein in activated lymphocytes from normal individuals was compared to that of contact dermatitis and CU patients. CD(40L) expression was found significantly higher on in (vitro activated CD3 [with phorbol myristate acetate (PMA) and ionomycine Ca2+ at 12 hr of culture] from CU patients compared to that of contact dermatitis and normal individuals. Whereas the proliferation of activated B cells from CU patients was higher, dexamethazone-induced inhibition of B cell proliferation was found statistically similar in both groups yet lower in B cells from most severe CU patients. We demonstrate a higher bcl-2 expression in activated B and T lymphocytes of severe CU patients compared to that of moderate CU and both contact dermatitis and normal individuals. The increased expression of CD(40L) on activated T cells might play a role in the polyclonal increased B cell proliferation of CU patients. This increased proliferation accompanies the finding that activated B and T lymphocytes from these patients demonstrate increased bcl-2 expression. The resistance of some B cells to dexamethazone-induced inhibition of proliferation encourages us to investigate the possibility that B cells from some CU patients might develop rescue mechanisms from activated cell death. These findings provide further evidence that CU is indeed an autoimmune disease, although its precise nature has yet to be fully elucidated.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0271-9142
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
371-8
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Immune aberrations in B and T lymphocytes derived from chronic urticaria patients.
pubmed:affiliation
Division of Clinical Immunology and Allergy, Bnai Zion Medical Center, Haifa, Israel.
pubmed:publicationType
Journal Article