Abstract
Basophils and mast cells have high affinity IgE receptors (FcεRI) on their plasma membrane and play important roles in FcεRI-associated allergic diseases, such as pollen allergy, food allergy, chronic spontaneous urticarial (CSU), and atopic dermatitis (AD). To date, several reports have revealed that high IgE antibody concentrations activate mast cells—which reside in tissue—in the absence of any antigens (allergens). However, IgE antibody-induced activation of basophils—which circulate in blood—has not been reported. Here, we investigated whether IgE antibodies may regulate functions of human peripheral basophils without antigens in vitro. We successfully removed IgE antibodies bound to FcεRI on the surface of human peripheral basophils by treating with 0.1% lactic acid. We also demonstrated that high IgE antibody concentrations (>1 μM) induced histamine release, polarization, and CD203c upregulation of IgE antibody-stripped basophils. Thus, high IgE antibody concentrations directly activate basophils, which express IgE-free FcεRI on the cell surface. This mechanism may contribute to the pathogenesis of patients with AD and CSU who have higher serum IgE concentrations compared to healthy donors.
Highlights
It is well known that basophils circulate in blood and account for less than 1% of peripheral blood leukocytes [1]
IL-3 and IL-3 receptors (IL-3R) interactions play an important role for enhancement of antigen-IgE antibody interaction-induced histamine release, development, and survival of basophil [3,5]
Sci. 2019, 20, 45 hand, peripheral basophils can be sensitized with just IgE antibodies when the concentrations of IgE antibodies in serum are low (Figure S2), and FcεRI on basophils can gradually become occupied by IgE antibodies in serum
Summary
It is well known that basophils circulate in blood and account for less than 1% of peripheral blood leukocytes [1]. Basophils express the high-affinity IgE receptors (FcεRI) and IL-3 receptors (IL-3R) on their surface [1,3,4]. IL-3 and IL-3R interactions play an important role for enhancement of antigen-IgE antibody interaction-induced histamine release, development, and survival of basophil [3,5]. Mast cells express FcεRIs on their surface and are activated in response to antigen-IgE antibody interactions, resulting in both the release of inflammatory mediators, such as histamines, and morphological changes [6]. SAUs sahroewsingninifiFcigaunrtelySh1aig, thheerctohnacnenthtroatsieonins osef rIagEofanhteibaoltdhiyesdionnsoerras.oMf poarteieonvtesr, the levelswoitfhIgAEDaonrtCibSoUdaieres siingnsiefricaaanrtleyphriogpheorrtthioannatlhtoosethinesleervaeolfohfeIagltEhyredcoenpotrosr.sM(ForceεoRvIe)r,etxhperleesvseelds oofn the surfaIcgeEoafnhtiubmodainespinersieprhaearraelpbraospooprthioilnsa(lFtiogtuhreeleSv1eal).of IgE receptors (FcεRI) expressed on the surface of human peripheral basophils (Figure S1a). Stripping of IgE Antibodies Bound to FcεRIs on the Surface of Human Peripheral Basophils. WWhhiitteebbaarrsshhoowwssccaa. .1100μμmm. .(b(b) )EExpxprersessisoinonlelveevleslos foCf DC2D0230c3ocnotnhethseusrufarcfeacoef obfasboapsohpilhs iilns rinesrpeosnpsoentsoe ItgoEIgaEntaibnotidbioeds i(e1s0(μ10g/μmg/Lm).L)
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