Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1998-4-9
pubmed:abstractText
B-CLL patients have a high prevalence of autoimmune phenomena due to polyclonal autoantibodies (Abs) restricted to blood cell self-antigens (Ag) and progressively develop a severe hypogammaglobulinemia. Autoimmunity and immunodeficiency have been related to B-CLL biological properties and cellular origin. Three major issues have emerged: 1) the relevance of B cell receptor abnormalities. More specifically, the importance of the defective expression of CD79b which may explain the faint to virtually undetectable amounts of monoclonal sig, the anomalous signal transduction and the failure to present antigens (Ag). 2) the possibility that the relentless accumulation of B-CLL cells is also under microenvironmental influences. These are brought about by the interplay of cytokines produced through cell/cell contacts among malignant B cells, macrophages and T cells. 3) the view that the very properties of accumulating anergic self-reactive CD5+ B lymphocytes may provide a bridge between autoimmunity and immune incompetence. CD5+ malignant B cells influence the cytokine production by T cells, but are inefficient Ag presenting cells (APC). As such they are a hurdle to the production of normal Ab. However, by stimulating in vitro the CD40 molecule on the membrane of CLL cell with the CD40 ligand the inefficient APC is turned into an efficient APC. In vivo, such an activation may conceivably occur in specific environments like the spleen and favour the production by normal residual B-cells of polyclonal autoAb against red cell or platelet self Ag.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1269-3286
pubmed:author
pubmed:issnType
Print
pubmed:volume
39 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S13-6
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Relationship between autoimmunity and immunodeficiency in CLL.
pubmed:affiliation
Dipartimento di Scienze Biomediche e Oncologia Umana, Università di Torino, Italy.
pubmed:publicationType
Review, Congresses