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2017 ; 8
(ä): 275
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Monomeric Immunoglobulin A from Plasma Inhibits Human Th17 Responses In Vitro
Independent of Fc?RI and DC-SIGN
#MMPMID28352269
Saha C
; Das M
; Patil V
; Stephen-Victor E
; Sharma M
; Wymann S
; Jordi M
; Vonarburg C
; Kaveri SV
; Bayry J
Front Immunol
2017[]; 8
(ä): 275
PMID28352269
show ga
Circulating immunoglobulins including immunoglobulin G (IgG) and IgM play a
critical role in the immune homeostasis by modulating functions of immune cells.
These functions are mediated in part by natural antibodies. However, despite
being second most abundant antibody in the circulation, the immunoregulatory
function of IgA is relatively unexplored. As Th17?cells are the key mediators of
a variety of autoimmune, inflammatory, and allergic diseases, we investigated the
ability of monomeric IgA (mIgA) isolated from pooled plasma of healthy donors to
modulate human Th17?cells. We show that mIgA inhibits differentiation and
amplification of human Th17?cells and the production of their effector cytokine
IL-17A. mIgA also suppresses IFN-? responses under these experimental conditions.
Suppressive effect of mIgA on Th17 responses is associated with reciprocal
expansion of FoxP3-positive regulatory T cells. The effect of mIgA on Th17?cells
is dependent on F(ab')(2) fragments and independent of Fc?RI (CD89) and DC-SIGN.
Mechanistically, the modulatory effect of mIgA on Th17?cells implicates
suppression of phosphorylation of signal transducer and activator of
transcription 3. Furthermore, mIgA binds to CD4(+) T cells and recognizes in a
dose-dependent manner the receptors for cytokines (IL-6R? and IL-1RI) that
mediate Th17 responses. Our findings thus reveal novel anti-inflammatory
functions of IgA and suggest potential therapeutic utility of mIgA in autoimmune
and inflammatory diseases that implicate Th17?cells.
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