Altered T cell and monocyte subsets in prolonged immune reconstitution inflammatory syndrome related with DRESS (drug reaction with eosinophilia and systemic symptoms)
10.5415/apallergy.2020.10.e2
- Author:
Sung Yoon KANG
1
;
Jihyun KIM
;
Jongho HAM
;
Sang Heon CHO
;
Hye Ryun KANG
;
Hye Young KIM
Author Information
1. Department of Internal Medicine, Gachon University Gil Medical Center, Incheon, Korea.
- Publication Type:Case Report
- Keywords:
DRESS syndrome;
Allopurinol;
Herpesviruses;
Immune reconstitution
- MeSH:
Allopurinol;
Drug Hypersensitivity Syndrome;
Eosinophilia;
Exanthema;
Herpesviridae;
Humans;
Immune Reconstitution Inflammatory Syndrome;
Middle Aged;
Monocytes;
Recurrence;
T-Lymphocytes;
T-Lymphocytes, Regulatory;
Th2 Cells
- From:
Asia Pacific Allergy
2020;10(1):2-
- CountryRepublic of Korea
- Language:English
-
Abstract:
Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a severe cutaneous adverse reaction involving various internal organs. Flare-ups after recovery from the initial presentation of DRESS are caused by relapse of drug-induced T-cell-mediated reactions. However, the specific underlying mechanism is unclear. Here, we report a case of a 60-year-old man with allopurinol-induced DRESS who suffered recurrent episodes of generalized rash with eosinophilia, which mimicked immune reconstitution inflammatory syndrome. Analysis of immunological profiles revealed that the percentages of T lymphocytes and regulatory T cells in the patient with DRESS were higher than those in healthy controls. In addition, there was a notable change in the subtype of monocytes in the patient with DRESS; the percentage of nonclassical monocytes increased, whereas that of classical monocytes decreased. Upon viral infection, nonclassical monocytes exhibited strong pro-inflammatory properties that skewed the immune response toward a Th2 profile, which was associated with persistent flare-ups of DRESS. Taken together, the results increase our understanding of the pathogenesis of DRESS as they suggest that expansion of nonclassical monocytes and Th2 cells drives disease pathogenesis.
