IIntravenous immunoglobulin modulates the number and function of low density neutrophils in patients with CVID

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Title in English Intravenous immunoglobulin modulates the number and function of low density neutrophils in patients with CVID
Authors

SLANINA Peter ŠTÍCHOVÁ Julie LITZMAN Jiří CHOVANCOVÁ Zita FRIČ Jan VLKOVÁ Marcela

Year of publication 2021
Type Conference abstract
MU Faculty or unit

Faculty of Medicine

Citation
Description Common variable immunodeficiency disorder (CVID) is the most common form of clinically significant primary immunodeficiency. Majority of patients receive intravenous immunoglobulin (IVIg) replacement therapy with potent immunomodulatory properties on individual components of the immune system. CVID is associated with chronic granulocytic activation and an increased percentage of Low Density Neutrophils (LDN) observed in the layer of peripheral blood mononuclear cells (PBMC). Changes in the percentage of LDN in PBMC and expression of their surface markers were studied in 25 CVID patients and 27 healthy donors (HD) in a whole blood sample and after in-vitro stimulation of whole blood with IVIg. We confirmed an increased number of LDN in the PBMC layer in a fresh blood sample from CVID patients. The LDN of patients and a HD group consisted of mature and immature neutrophils distinguished based on the expression of CD10 and CD16. Stimulation of whole blood with IVIg caused an increase of LDN in both CVID patients and HD. This enhancement in LDN was caused by mature neutrophils CD16+CD10+ in both groups. The suppressive effect of induced LDN on T-cell proliferation was confirmed. Flow cytometry measurements revealed altered expression of CD274 and CD10 on mature LDN of CVID patients. The addition of IVIg inhibited the expression of CD11b on the mature LDN in both experimental groups. These results indicate that IVIg supports the formation of LDN, which can negatively affect the immune response and can significantly contribute to the chronic inflammation observed in patients with CVID.
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