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Erik R. Hansen, MD; Steen Lisby; Ole Baadsgaard, MD; Vincent C. Ho, MD, FRCPC; E.-M. de Villiers, PhD; Gunhild L. Vejlsgaard, PhD

Arch Dermatol. 1990;126(12):1604-1608.

Abstract
• Human papillomavirus-induced infections may be associated with cellular immunodeficiency. However, very little is known about the dysfunctional interactions among T lymphocytes, B lymphocytes, and antigen-presenting cells. A 30-year-old heterosexual man with a 10-year history of persistent multiple refractory flat wart lesions containing human papillomavirus type 3-related DNA sequence was studied. The patient had a severe depletion of CD4⁺ T lymphocytes and a compensatory increase in the number of CD8⁺ T lymphocytes. Impaired T-lymphocyte response to various stimuli was found. Depletion of the increased number of CD8⁺ T lymphocytes, which suppressed immunoglobulin production in vitro, did not restore the impaired T-lymphocyte response. Immobilized anti-CD3 beads that stimulate the T lymphocyte antigen complex in the absence of antigen-presenting cells indicated a T-lymphocyte defect, rather than a decreased antigen-presenting cell function. Thus, the pronounced cellular immunodeficiency was due to abnormal function of the CD4⁺ helper/inducer T lymphocytes.

(Arch Dermatol. 1990;126:1604-1608)

Author Affiliations
From the Immunology Laboratory, Department of Dermatology, University Hospital, Copenhagen, Denmark (Drs Hansen, Lisby, and Vejlsgaard), Department of Dermatology, University of Michigan, Ann Arbor (Drs Ho and Baadsgaard), and Deutsches Krebsforschungszentrum, Referenzzentrum für humanpathogene Papillomviren, Heidelberg, Germany (Dr de Villiers).

Footnotes
Accepted for publication August 6, 1990.

Reprint requests to Laboratory of Immunology, Department of Dermatology, University Hospital, Blegdamsvej 9, DK 2100 Copenhagen 0 Denmark (Dr Hansen).

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