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2017 ; 17
(5
): 352-364
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Functional Defects in Type 3 Innate Lymphoid Cells and Classical Monocytes in a
Patient with Hyper-IgE Syndrome
#MMPMID29093656
Chang Y
; Kang SY
; Kim J
; Kang HR
; Kim HY
Immune Netw
2017[Oct]; 17
(5
): 352-364
PMID29093656
show ga
Hyper-IgE syndrome (HIES) is a very rare primary immune deficiency characterized
by elevated serum IgE levels, recurrent bacterial infections, chronic dermatitis,
and connective tissue abnormalities. Autosomal dominant (AD) HIES involves a
mutation in signal transducer and activator of transcription 3 (STAT3) that leads
to an impaired T(H)17 response. STAT3 signaling is also involved in the function
of ROR?t(+) type 3 innate lymphoid cells (ILC3s) and ROR?t(+)T(H)17 cells. The
aim of this study was to investigate the role of innate immune cells such as
innate lymphoid cells (ILCs), granulocytes, and monocytes in a patient with HIES.
Peripheral blood mononuclear cells (PBMCs) from a patient with HIES and three
age-matched healthy controls were obtained for the analysis of the innate and
adaptive immune cells. The frequencies of ILCs in PBMCs were lower in the patient
with HIES than in the controls. Moreover, granulocyte-macrophage
colony-stimulating factor (GM-CSF) and IL-17A produced by ILC3s in PBMCs were
lower in the patient with HIES than the controls. Compared with the controls,
classical monocytes (CD14(+)CD16(low)), which have a high antimicrobial
capability, were also lower in the patient with HIES, while non-classical
monocytes (CD14(low)CD16(+)) as well as intermediate monocytes
(CD14(+)CD16(intermediate)) were higher. Taken together, these results indicate
that the impaired immune defense against pathogenic microbes in the patient with
HIES might be partially explained by functional defects in ILC3s and inflammatory
monocytes.
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