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J. Scott Kasteler, MD; Marta J. Petersen, MD; Jerome E. Vance, MD; John J. Zone, MD

Arch Dermatol. 1992;128(6):795-798.

Abstract
• Background and Design.—
Autoeczematization, the symmetric diffuse spread of a previously localized dermatitis, has an unclear etiology although some investigators have postulated that activated T lymphocytes play a role. Two estimates of activation of peripheral T lymphocytes are the cell surface expression of the HLA-DR antigen and the interleukin 2 receptor (IL-2R). We measured the percentage of circulating activated T lymphocytes in nine patients with autoeczematization compared with normal controls (n=10), patients with stasis dermatitis (n=6), and patients with severe (n=10) or mild (n=8) psoriasis. The percentage of activated T lymphocytes was determined by fluorescent, activated cell sorter analysis of peripheral leukocytes doubly stained with antibodies to T lymphocytes and HLA-DR antigen or IL-2R.

Results.—
Statistically significant elevations of HLA-DR- and IL-2R-positive T lymphocytes were seen in autoeczematization patients (P<.004 and P<.04, respectively) and those with severe psoriasis (P<.004 for HLA-DR antigen and IL-2R). Percentages of HLA-DR- and IL-2R-positive T lymphocytes in patients with mild psoriasis were not significantly elevated. Two patients with autoeczematization had a reduction of their previously elevated levels of HLA-DR- and IL-2R-positive T lymphocytes after treatment.

Conclusions.—
These data suggest a possible role for circulating activated T lymphocytes in the pathogenesis of autoeczematization and possibly in severe psoriasis.

(Arch Dermatol. 1992;128:795-798)

Author Affiliations
From the Division of Dermatology, Department of Internal Medicine, Salt Lake City (Utah) Veterans Affairs Medical Center (Dr Zone); and the Division of Dermatology, University of Utah School of Medicine, Salt Lake City (Drs Kasteler, Petersen, Vance, and Zone). Read in part before the Western Meeting of the American Federation of Clinical Research, Carmel, Calif, February 7, 1991.

Footnotes
Accepted for publication November 6, 1991.

Reprint requests to the Division of Dermatology, University of Utah Health Sciences Center, 50 N Medical Dr, Salt Lake City, UT 84132 (Dr Petersen).

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