Identifying Toll-like receptor expression in cutaneous sarcoidosis.

Toll-like receptors (TLRs) are known to be expressed in the skin. Antigenic stimulation of TLRs in the skin has been implicated in several inflammatory dermatologic diseases including psoriasis, syphilis, atopic dermatitis, and cutaneous T-cell lymphoma. However, the expression of TLRs in cutaneous sarcoidosis has not yet been defined. Expression of TLRs 1-9 was examined in cutaneous sarcoid by immunohistochemical staining. It was found that TLRs 5 and 6 stained most intensely in both the granulomas and epidermis of the sarcoid cases. TLRs 2, 3, 4, 7, and 8 stained more intensely compared with normal skin. All sarcoidosis cases showed an increased level of staining compared with the control. The nuclear factor-kappa B activation pathway was confirmed by staining for p65. All cases strongly stained for p65 in the granulomas and varied in staining intensity in the epidermis. The identified TLR expression in cutaneous sarcoidosis indicates that a bacterial antigen could be an etiologic agent of the disease. Future studies that clearly define the etiology of sarcoid will lead to better therapies and a better prognosis for affected patients.

Etanercept-induced cystic acne.

Tumor necrosis factor α antagonists are potent biologics used to treat a variety of autoimmune disorders such as rheumatoid arthritis, ankylosing spondylitis, Crohn disease, psoriasis, and psoriatic arthritis. These medications are known to have many side effects (eg, infusion reactions, cytopenia, risk for infection, heart failure); however, only a few cases of acne vulgaris have been associated with the use of these biologics, particularly infliximab and adalimumab. We report a rare case of etanercept-induced cystic acne.

A case of idiopathic follicular mucinosis treated with bexarotene gel.

BACKGROUND: Topical bexarotene 1% gel is currently FDA-approved for early stage (IA and IB) persistent or refractory cutaneous T-cell lymphoma (CTCL). No uniformly effective therapy exists for follicular mucinosis, although several treatments are routinely used. There are no known reports of topical bexarotene being used in the treatment of idiopathic follicular mucinosis when there is no association with CTCL. This article reports the first case of bexarotene gel to successfully treat persistent idiopathic follicular mucinosis. MATERIALS AND METHODS: This study describes a 34-year-old Caucasian male with idiopathic follicular mucinosis. The patient had treatment failure with clobetasol 0.05% ointment and narrow-band UVB. Intralesional injections with triamcinolone 5 mg/ml were successful for treating the plaques in the beard area. The patient was treated with bexarotene 1% gel applied twice a day to the persistent plaques on the lower extremities. The patient reported significant improvement in hair growth after only six weeks of treatment. The treatment was decreased to once a day due to erythema, and he had complete hair regrowth at 26 weeks. DISCUSSION: Several treatments have been described in the literature, such as corticosteroids, psoralen plus ultraviolet A (PUVA) light therapy, topical nitrogen mustard, and radiation therapy. Isolated cases have documented the beneficial responses of pimecrolimus, dapsone, indomethacin, minocycline, isotretinoin, hydroxychloroquine and interferons. No single treatment has been shown to be consistently effective. CONCLUSION: Topical bexarotene 1% gel should be considered for patients with idiopathic follicular mucinosis resistant to standard treatment.

Mapping Toll-like receptor activity in different stages of cutaneous T-cell lymphoma.

It is known that human keratinocytes (KCs) express Toll-like receptors (TLRs). However, published reports conflict regarding TLR expression in cutaneous T-cell lymphoma patient's KCs. To define the pattern of expression and detect any differences of TLRs 1-9 and p65 expression in epidermal KCs, tumor infiltrate, and endothelial cell types using immunohistochemical stains on fixed and paraffin-embedded sections of mycosis fungoides (MF) in patch, plaque, and nodular stages. MF cases showed no change in pattern of TLRs expressed through different stages but increased epidermal staining of TLRs 2, 3, 4, 5, 6, and 8 with higher scores associated with more aggressive stages. Endothelial cell staining was increased for TLR 4 and 6. Tumor infiltrate staining was strongest with TLRs 5 and 7. Individual cases with disease progression showed increased intensity of TLRs 4, 5, and 6 staining in the epidermis, tumor infiltrate, and endothelial cell. p65 verified nuclear factor kappa B activation of the TLR pathway with trace staining of the epidermis and 1-2+ staining of tumor infiltrate. MF cases showed increased epidermal expression of TLRs and increased endothelial cell staining compared with controls. TLR expression may be driven by antigenic stimulation and may play a role in the activation of neoplastic T cells in the skin. Further definition of TLR patterns may refine the use of TLR modifiers for treatment.