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Title: The impact of supplementary doses of intravenous immunoglobulins preparations on the number and pro-inflammatory response of CD14+CD16++ monocytes


The aim of the study was to estimate the numbers of CD14+CD16++ monocytes (as the main producers of TNF) and their proinflammatory response in patients with primary humoral immunodeficiencies (PID). The influence of IVIG preparations applied as a supplementary therapy in CVID subjects, on the numbers and activity of CD14+CD16++ cells was also evaluated. Finally, a possible mechanisms of these activities were studied. Numbers of “non classical” CD14+CD16++ monocytes were evaluated in adult and pediatric patients with PID. Impact of intravenous immunoglobulins (IVIG; 0,4 g/kg body weight) on monocyte subpopulations and cytokine production was studied in adult patients with CVID supplemented with IVIG. Monocyte numbers did not show any abnormalities in studied humoral immunodeficiences patients. In adults CVID patients decrease of CD14+CD16++ by about 50% at 4 h after beginning of IVIG was observed. At the same time, levels of TNF and IL-12p70 in the supernatants of stimulated PBMC isolated from patients decreased significantly. The numbers of CD14+CD16++ cells returned to the basic level in app. 20 h after beginning of IVIG. The intracellular expression of TNF in stimulated (LPS) ex vivo non classical monocytes also decreased in some patients at 4 h after beginning of IVIG. CD14+CD16++ monocytes, in comparison to CD14++CD16-, showed app. two-fold higher expression of FcγRIIB(CD32B). Triggering of FcγRIIB with IVIG during in vitro performed experiments also caused inhibition of TNF production following 4 h lasting LPS stimulation, preferentially in CD14+CD16++ cells obtained from healthy blood donors.

Level of degree:

2 - studia doktoranckie

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Degree grantor:

Wydział Lekarski


Maciej Siedlar

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tylko w bibliotece

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Biblioteka Medyczna Uniwersytetu Jagiellońskiego - Collegium Medicum

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Last modified:

Oct 7, 2019

In our library since:

Nov 21, 2012

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Edition name Date
ZB-112126 Oct 7, 2019


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