Preparations of intravenous immunoglobulins diminish the number and proinflammatory response of CD14+CD16++ monocytes in common variable immunodeficiency (CVID) patients

Maciej Siedlar; Magdalena Strach; Karolina Bukowska-Strakova; Marzena Lenart; Anna Szaflarska; Kazimierz Węglarczyk; Magdalena Rutkowska; Monika Baj-Krzyworzeka; Anna Pituch-Noworolska; Danuta Kowalczyk; Tomasz Grodzicki; Loems Ziegler-Heitbrock; Marek Zembala

doi:10.1016/j.clim.2011.01.002

Preparations of intravenous immunoglobulins diminish the number and proinflammatory response of CD14+CD16++ monocytes in common variable immunodeficiency (CVID) patients

Clin Immunol. 2011 May;139(2):122-32. doi: 10.1016/j.clim.2011.01.002. Epub 2011 Jan 15.

Authors

Maciej Siedlar¹, Magdalena Strach, Karolina Bukowska-Strakova, Marzena Lenart, Anna Szaflarska, Kazimierz Węglarczyk, Magdalena Rutkowska, Monika Baj-Krzyworzeka, Anna Pituch-Noworolska, Danuta Kowalczyk, Tomasz Grodzicki, Loems Ziegler-Heitbrock, Marek Zembala

Affiliation

¹ Department of Clinical Immunology, Polish-American Institute of Pediatrics, Jagiellonian University Medical College, Krakow, Poland. misiedla@cyf-kr.edu.pl

PMID: 21300572
DOI: 10.1016/j.clim.2011.01.002

Abstract

We have studied the effect of intravenous immunoglobulins (IVIG) on monocyte subpopulations and cytokine production in patients with CVID. The absolute number of CD14(+)CD16(++) monocytes decreased on average 2.5-fold 4h after IVIG and after 20h returned to the baseline. The cytokine level in the supernatants of peripheral blood mononuclear cells (PBMC) after ex vivo LPS stimulation demonstrated the >2-fold decrease in TNF production 4h after IVIG. The TNF expression, which is higher in the CD14(+)CD16(++) monocytes, was decreased in these cells by IVIG in 4/7 CVID cases. In vitro exposure of the healthy individuals' monocytes to the IVIG preparation resulted in reduced TNF production, which was overcome by blockade of the FcγRIIB in the CD14(+)CD16(++) CD32B(high) monocytes. Our data suggest that reduction in the number of CD14(+)CD16(++) monocytes and the blockade of their cytokine production via triggering CD32B can contribute to the anti-inflammatory action of IVIG.

Publication types

Clinical Trial
Research Support, Non-U.S. Gov't

MeSH terms

Adult
Antibodies, Monoclonal / pharmacology
Antigens, CD / metabolism
Common Variable Immunodeficiency / therapy*
Female
GPI-Linked Proteins / metabolism
HLA-DR Antigens / metabolism
Humans
Immunoglobulins, Intravenous / pharmacology*
Immunoglobulins, Intravenous / therapeutic use
Immunophenotyping
Interleukin-10 / metabolism
Interleukin-12 / metabolism
Kinetics
Leukocyte Count
Leukocytes, Mononuclear / drug effects
Leukocytes, Mononuclear / metabolism
Lipopolysaccharide Receptors / metabolism*
Lipopolysaccharides / pharmacology
Male
Middle Aged
Monocytes / cytology
Monocytes / drug effects*
Monocytes / immunology
Monocytes / metabolism
Receptors, IgG / immunology
Receptors, IgG / metabolism*
Tumor Necrosis Factor-alpha / metabolism
Young Adult

Substances

Antibodies, Monoclonal
Antigens, CD
FCGR3B protein, human
Fc gamma receptor IIB
GPI-Linked Proteins
HLA-DR Antigens
IL10 protein, human
Immunoglobulins, Intravenous
Lipopolysaccharide Receptors
Lipopolysaccharides
Receptors, IgG
Tumor Necrosis Factor-alpha
Interleukin-10
Interleukin-12