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Increased serum levels of soluble IL‐2 receptor, CD30 and CD8 molecules, and gamma‐interferon in angioimmunoblastic lymphadenopathy: possible pathogenetic role of immunoactivation mechanisms
Author(s) -
Pizzolo G.,
Stein H.,
JosimovicAlasevic O.,
Vinante F.,
Zanotti R.,
Chilosi M.,
Feller A. C.,
Diamantstein T.
Publication year - 1990
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1990.tb07786.x
Subject(s) - cd8 , interferon gamma , receptor , immunology , cd30 , medicine , pathology , chemistry , cancer research , lymphoma , cytokine , immune system
S ummary . Abnormal immunoreaction associated with increased cell activation phenomena might play a role in the pathogenetic events leading to the development of angioimmunoblastic lymphadenopathy (AILD). In the present study we investigated the serum levels of some soluble molecules related to cell activation in 24 patients with AILD at presentation. In particular, we measured by immunoenzymatic or immunoradiometric techniques the levels of the Tac peptide (sIL‐2R), soluble CD30 (sCD30) and CD8 (sCD8) antigens, and gamma‐IFN (gIFN). The results show that all the above molecules are increased as compared to normal controls, with a different pattern of increase for the different molecules. The sIL‐2R levels were very high in all cases with no overlap between AILD and control samples (mean 6315±3374 U/ml, controls 271±112 U/ml, P <0.001). Very high values of the sCD30 antigen (722±895 U/ml) were detected in all cases but five, as opposed to the lack of detectable levels in controls. A significant increase of sCD8 (978±646 U/ml, controls 334±95 U/ml, P <0.01) and gIFN (329±236 U/ml, controls 97±43 U/ml, P <0.01) was also observed with some overlap between AILD samples and controls. The above findings further support the view that a condition of abnormally enhanced cell activation is likely to play a central role in the pathogenetic events leading to the composite clinicopathological picture of AILD.