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Th2 cytokine mRNA expression in primary cutaneous CD30-positive lymphoproliferative disorders: successful treatment
1Department of Dermatology, Hamamatsu University School of Medicine, Japan.
Insights
Primary cutaneous CD30-positive lymphoproliferative disorders, including KiL and LyP type A, exhibit a Th2 cytokine profile. Recombinant interferon-gamma (rIFN-gamma) effectively reduced CD30+ cells and improved lesions by downregulating cytokine mRNA.
Area of Science:
- Dermatology
- Immunology
- Oncology
Background:
- Primary cutaneous CD30-positive lymphoproliferative disorders encompass KiL and LyP type A.
- These disorders are characterized by skin-infiltrating CD30+ cells.
Purpose of the Study:
- To investigate the cytokine profile of skin-infiltrating cells in primary cutaneous CD30-positive lymphoproliferative disorders.
- To evaluate the therapeutic efficacy of recombinant interferon-gamma (rIFN-gamma) in these conditions.
Main Methods:
- Cytokine mRNA expression (IL-4, IL-10, IL-2, IFN-gamma) in skin lesions was analyzed using reverse transcriptase-polymerase chain reaction.
- A predictive skin test with local rIFN-gamma injection was performed.
- Therapeutic efficacy of rIFN-gamma was assessed via intravenous or local administration.
Main Results:
- Skin lesions from KiL and LyP patients showed elevated IL-4 and IL-10 mRNA, unlike normal skin.
- A predictive skin test indicated that rIFN-gamma could downregulate IL-4 and IL-10 mRNA and decrease CD30+ cells in responsive patients.
- Three out of four patients who responded to the skin test showed objective improvement and reduced CD30+ cells after rIFN-gamma therapy.
Conclusions:
- Skin-infiltrating CD30+ cells in KiL and LyP possess a Th2 cytokine profile.
- rIFN-gamma therapy holds promise for treating these disorders by inhibiting cytokine production and CD30+ cell proliferation.
Abstract:
Primary cutaneous CD30 (Ki-1)+ large cell lymphoma (KiL) and lymphomatoid papulosis (LyP) type A are collectively termed as primary cutaneous CD30-positive lymphoproliferative disorders. We examined the cytokine profile of skin-infiltrating cells and the therapeutic efficacy of recombinant interferon-gamma (rIFN-gamma) in primary cutaneous KiL and LyP type A. By reverse transcriptase-polymerase chain reaction, mRNAs for interleukin-4 (IL-4) and IL-10 were detected in the dermis of skin lesions in all cases (three cases of KiL and four cases of LyP). In addition, tissue from one KiL patient transcribed IL-2 and IFN-gamma messages, and one LyP patient showed IL-2 mRNA. In contrast, normal skin from ten healthy donors contained mRNA for IL-2 or IFN-gamma, or both, but not for IL-4. Before the therapeutic trial of rIFN-gamma, the response of skin lesions was assessed by a predictive skin test with local injection of rIFN-gamma (0.5 x 10(6) Japan Reference Units [JRU; 1 JRU roughly corresponds to 4 NIH units]) for 3 consecutive days in two KiL and two LyP patients. Numbers of skin-infiltrating CD30+ cells were decreased, and transcription of mRNA for IL-4 and IL-10 was downregulated after the skin test in one KiL and two LyP cases. One KiL patient showed no histologic response or change in mRNA expression. In the therapeutic trial, rIFN-gamma (total doses of 1.2-4.0 x 10(7) JRU) was administered intravenously (n = 2) or locally (n = 2). In three patients who responded to the skin test, the lesions were objectively improved and the numbers of skin-infiltrating CD30+ cells were markedly decreased after the therapeutic trial. No improvement was observed in one KiL patient who did not respond to the skin test. These findings suggest that the skin-infiltrating CD30+ cells in KiL and LyP have a Th2 cytokine profile and raise the possibility that the administration of rIFN-gamma improves the conditions by inhibiting cytokine mRNA transcription and proliferation of CD30+ cells.
