Characterization of monocyte subtypes in the allergic form of atopic eczema/dermatitis syndrome.
BACKGROUND
Monocyte (Mo) subsets exhibiting distinct phenotypic and functional properties identified in peripheral blood are assumed to be under the control of soluble factors from their surrounding micromilieu. Atopic eczema/dermatitis syndrome (AEDS) is accompanied by humoral and cellular alterations among which an increased expression of the high-affinity receptor for IgE (Fc epsilon RI) on antigen presenting cells, like Mo, could be found. Therefore we analyzed the assembly of circulating Mo populations and their Fc epsilon RI surface expression during the course of AEDS.


METHODS
Blood samples were taken from AEDS patients before and after topical treatment as well as from psoriasis patients and healthy control donors. Detailed analysis of Mo subsets was done by flow cytometry. Meticulous clinical scoring included quantification of the surface damage using the eczema area and severity index (EASI score) as well as evaluation of the serum level of thymus- and activation-regulated chemokine (TARC); this was done before and after 2 weeks of topical treatment with tacrolimus ointment 0.1%.


RESULTS
During the exacerbation phase of AEDS, patients harboured a different assembly of Mo subtypes from normal nonatopic individuals and patients with psoriasis with a significant increased population of CD14(+)CD64(-) CD16(+) Mo. Clinical improvement led to a significant decrease of this subpopulation in favor of CD14(+)CD64(+)CD16(-) Mo, leading to a composition of Mo subsets similar to the state found in healthy donors. Interestingly, Fc epsilon RI expression was confined to the CD14(+)CD64(+)CD16(-) Mo subpopulation and the percentage of this Fc epsilon RI(+) Mo subset increased significantly in the peripheral blood after topical treatment.


CONCLUSIONS
Our data provide for the first time clear evidence that fluctuations of Mo subsets in AEDS might reflect qualitatively and quantitatively distinct contributions of Mo subsets to the development of AEDS.
Novak
N
N
Department of Dermatology, Friedrich-Wilhelms University, D-53105 Bonn.
Allam
P
P
Geiger
E
E
Bieber
T
T
D000328:Adult; D015703:Antigens, CD / Q000032:analysis / Q000097:blood; D054414:Chemokine CCL17; D019742:Chemokines, CC / Q000097:blood; D003872:Dermatitis / Q000097:blood* / Q000150:complications*; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000145:classification*; D010641:Phenotype; D011565:Psoriasis / Q000097:blood* / Q000150:complications*; D017455:Receptors, IgE / Q000096:biosynthesis; D012720:Severity of Illness Index; D013577:Syndrome; D013997:Time Factors
D015703:Antigens, CD; C106230:CCL17 protein, human; D054414:Chemokine CCL17; D019742:Chemokines, CC; D017455:Receptors, IgE; D007073:Immunoglobulin E