Chronic immune activation in common variable immunodeficiency ( CVID ) is associated with elevated serum levels of soluble CD 14 and CD 25 but not endotoxaemia
Author(s) -
Litzman J.,
Nechvatalova J.,
Xu J.,
Ticha O.,
Vlkova M.,
Hel Z.
Publication year - 2012
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.2012.04655.x
Subject(s) - common variable immunodeficiency , immunology , immune system , cd14 , lipopolysaccharide , antibody , t cell , immunodeficiency , il 2 receptor , biology , medicine
Summary Common variable immunodeficiency ( CVID ), the most frequent symptomatic immunoglobulin primary immunodeficiency, is associated with chronic T cell activation and reduced frequency of CD 4 + T cells. The underlying cause of immune activation in CVID is unknown. Microbial translocation indicated by elevated serum levels of lipopolysaccharide and soluble CD 14 ( sCD 14) has been linked previously to systemic immune activation in human immunodeficiency virus/acquired immune deficiency syndrome ( HIV ‐1/ AIDS) , alcoholic cirrhosis and other conditions. To address the mechanisms of chronic immune activation in CVID , we performed a detailed analysis of immune cell populations and serum levels of sCD 14, soluble CD 25 ( sCD 25), lipopolysaccharide and markers of liver function in 35 patients with CVID , 53 patients with selective immunoglobulin ( Ig)A deficiency ( IgAD ) and 63 control healthy subjects. In CVID subjects, the concentration of serum sCD 14 was increased significantly and correlated with the level of sCD 25, C ‐reactive protein and the extent of T cell activation. Importantly, no increase in serum lipopolysaccharide concentration was observed in patients with CVID or IgAD . Collectively, the data presented suggest that chronic T cell activation in CVID is associated with elevated levels of sCD 14 and sCD 25, but not with systemic endotoxaemia, and suggest involvement of lipopolysaccharide‐independent mechanisms of induction of sCD 14 production.
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