No abstract

The spectrum of the clinical manifestation and the course of folliculotropic mycosis fungoides are broad and differ from classic mycosis fungoides. Folliculotropic neoplastic T-cell proliferation is associated with activation of inflammatory reactive T- and B-lymphoid cells, mesenchymal cells and changes in the hair follicle.

Tissue-specific migration of immune cells involved both in physiological and pathological immune responses is a current research subject for medical science. Several homing molecules have been identified orchestrating extravasation of immune cells to certain peripheral non-lymphoid tissues such as gut, lung and skin. Regarding lymphocyte homing to skin, the first-line defense of human body cutaneous lymphocyte associated antigen (CLA) and a group of chemokine-chemokine receptor pairs are considered to be of crucial importance. The aim of the present review is to summarize existing knowledge about skin- and tumor-specific migration of immune cells playing a major pathogenetic role in host immune responses induced by non-lymphoid malignant skin tumors as well as in the development of primary cutaneous T-cell lymphomas (CTCL). Melanoma malignum, squamous and basal cell carcinoma evoke host immune responses and consequently a subset of reactive immune cells is recruited to site of the tumor. Regarding migratory process and exact functional role of these cells a growing number of data is available in literature. On the other hand tissue-specific immune cell homing is regarded as a key process in the pathogenesis of CTCL where malignant T-lymphocytes can be found in circulation and symptomatic skin. Hereby homing mechanism of malignant T-cells in mycosis fungoides and Sézary-syndrome as separate clinical entities of CTCL is discussed. A precise insight into the molecular background of skin- and tumor-specific immune cell migration can contribute to developing efficient vaccine therapies in non-lymphoid malignant skin tumors and beneficial treatment modalities in CTCL.

system and IL-13, IL-17E/IL-25 as well as COX-2 might be key factors to aggravate Ag-induced AD-like symptoms. AcknowledgementsThis study was supported by a grant from the Korean Healthcare technology R&D Project, Ministry for Health, Welfare & Family Affairs, Republic of Korea (A091121). Author contributionsJi-Yun Kim performed the research, designed the research study, analysed the data and wrote the paper; Mi Sook Jeong performed the research and analysed the data; Kui Young Park designed the research study and analysed the data; Seong Jun Seo designed the research study, analysed the data and wrote the paper. Ethics approval for animal careAll experiments with mice were performed in accordance with the regulations and the approval of the Institutional Animal Care and Use Committee of Chung-Ang University (Approval No. 10-1011) and Korea Conformity Laboratories (KCL). Conflict of interestsThe authors have declared no conflicting interests. Supporting InformationAdditional Supporting Information may be found in the online version of this article: Data S1. Supplementary Materials and Methods. Figure S1. Effects of FA inhalation on the clinical skin severity score and the infiltration of inflammatory cells in ear skin of NC/Nga mice. Table S1. Effect of FA inhalation on the production of total levels of immunoglobulin (Ig) isotypes in plasma. Table S2. Effect of FA inhalation on the protein expressions of cytokines in splenocytes. Abstract: A considerable number of patients with psoriasis show secondary resistance during long-term TNF-alpha inhibitor therapy, necessitating the identification of reliable predictive markers. Predictive role of cutaneous lymphocyte-associated antigen (CLA) was investigated. Thirty-eight severe patients with psoriasis were treated for a 24-week-long study period. Clinical responsiveness (PASI) and changes in flow cytometry-measured peripheral lymphocyte CLA expression (week 0-2-6) were statistically analysed. Regarding 24-week-long treatment outcome patients were divided into two groups: During the first 6 weeks, mean CLA expression showed significant (P = 0.034604) increase among responders (32/38), while after a preliminary increase, it was significantly (P = 0.012539) decreasing in the relapsing group (6/38). Pearson's correlation analysis showed significant negative correlation between PASI and CLA changes. Responders showed (not significantly) lower initial CLA expression than relapsing patients. Our observations suggest change in CLA expression during the first 6 weeks of induction period to serve as a potential predictive marker of TNF-alpha inhibitor therapy in psoriasis.

No abstract