Activated Leukocyte Cell Adhesion Molecule Modulates Th2 Immune Response in Atopic Dermatitis

PURPOSE: Activated leukocyte cell adhesion molecule (ALCAM), a member of the immunoglobulin superfamily, is highly expressed on dendritic cells. ALCAM and its receptor CD6 are co-stimulatory molecules in the immunological synapse; their interaction is required for T cell activation. While atopic dermatitis (AD) is recognized as a T helper 2 (Th2)-mediated allergic disease, the role of ALCAM in its pathogenesis is unclear. METHODS: ALCAM levels were measured in the serum of AD patients and AD-induced murine model by ovalbumin treatment. We next investigated transepidermal water loss, clinical score, Th2-immune responses, skin barrier gene expression and T-cell activation using wild-type (WT) and ALCAM deficiency mice. An oxazolone-induced AD-like model was also established and analyzed using WT- and ALCAM-deficient mice. RESULTS: We found that serum ALCAM levels were elevated in pediatric AD patients as well as WT AD mice, whereas Th2-type cytokine production and AD symptoms were suppressed in ALCAM-deficient mice. In addition, CD4+ effector T-cell counts in murine skin and skin-draining lymph nodes were lower in ALCAM-deficient mice than in their WT counterparts. ALCAM deficiency was also linked to higher expression of skin barrier genes and number of lamellar bodies. CONCLUSIONS: These findings indicate that ALCAM may contribute to AD pathogenesis by meditating a Th2-dominant immune response and disrupting the barrier function of the skin.

Pathophysiology of immune thrombocytopenic purpura: a bird's-eye view

Immune thrombocytopenic purpura [FTP] is a common autoimmune disorder resulting in isolated thrombocytopenia. It is a bleeding disorder characterized by low platelet counts due to decreased platelet production as well as increased platelet destruction by autoimmune mechanisms. ITP can present either alone [primary] or in the setting of other conditions [secondary] such as infections or altered immune states. ITP is associated with a loss of tolerance to platelet antigens and a phenotype of accelerated platelet destruction and impaired platelet production. Although the etiology of FTP remains unknown, complex dysregulation of the immune system is observed in ITP patients. Antiplatelet antibodies mediate accelerated clearance from the circulation in large part via the reticuloendothelial [monocytic phagocytic] system. In addition, cellular immunity is perturbed and T-cell and cytokine profiles are significantly shifted toward a type 1 and Thl7 proinflammatory immune response with impaired regulatory compartment, including Tregs and Bregs, have been reported, suggesting a generalized immune dysregulation in ITP. Understanding how Thl/Thl7/Treg differentiation and expansion are controlled is central to uncovering how autoimmunity may be sustained in ITP

Gene Expression Pattern of Human Chorion-Derived Mesenchymal Stem Cells during Adipogenic Differentiation

PURPOSE: The aim of this study was to identify the adipocyte-specific gene expression patterns in chorion-derived mesenchymal stem cells during adipogenic differentiation. MATERIALS AND METHODS: Chorionic cells were isolated from the third trimester chorions from human placenta at birth and identified morphologically and by fluorescence-activated cell sorting analysis. After inducing adipogenic differentiation for 28 days, cells at days 3, 10, 21 and 28 were analyzed by Oil red O staining and RNA extraction in order to assess the expression levels of adipocyte marker genes, including CCAAT-enhancer binding protein alpha (C/EBPalpha), peroxisome proliferator-activated receptor gamma (PPARgamma), fatty acid binding protein 4 (FABP4) and Glycerol-3-phosphate dehydrogenase (GPD2). Cells not induced for differentiation were compared with the induced cells as a control group. RESULTS: Chorion-derived cells showed the same pattern as fibroblasts, and expressed CD73, CD105, and CD166 antigens, but not CD45, CD34, and HLA-DR antigens. On day 3 after differentiation, cells began to stain positively upon Oil red O staining, and continuously increased in lipid granules for 4 weeks. The expression level of C/EBPalpha increased 4.6 fold on day 3 after induction, and continued to increase for 4 weeks. PPARgamma was expressed at a maximum of 2.9 fold on day 21. FABP4 and GPD2 were significantly expressed at 4.7- and 3.0-fold, respectively, on day 21, compared to controls, and further increased thereafter. CONCLUSION: Human chorion-derived mesenchymal stem cells exhibited the sequential expression pattern of adipocyte marker genes during differentiation, corresponding to adipogenesis.

Gene expression patterns induced by taxol(R) and cyclosporin a in oral squamous cell carcinoma cell line using cDNA microarray

Expression and significance of activated leukocyte cell adhesion molecule in prostatic intraepithelial neoplasia and adenocarcinoma / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the expression of activated leukocyte cell adhesion molecule(ALCAM) protein in prostatic intraepithelial neoplasia and adenocarcinoma, and the relationship between ALCAM expression and clinicopathological features of prostatic carcinoma.</p><p><b>METHODS</b>ALCAM protein expression was evaluated in the tissues of 41 human prostatic carcinomas by using immunohistochemistry (EnVision method).</p><p><b>RESULTS</b>ALCAM was widely expressed in prostatic epithelia. Overexpression of ALCAM was found in most prostatic intraepithelial neoplasias and low-grade cancers, whereas a decreased expression shown in some high-grade cancers. The ALCAM protein expression in prostatic carcinoma was correlated with pathological grading. However, no correlation of ALCAM expression was found with preoperative serum prostate-specific antigen levels or clinical stages.</p><p><b>CONCLUSION</b>Expression of ALCAM is disturbed in prostatic intraepithelial neoplasia and adenocarcinoma, indicating its involvement in the development of human prostatic carcinoma.</p>

Circulating levels of soluble scavenger receptors [SCD5 and SCD6] in primary and secondary Sjogren syndrome patients

To determine the existence of circulating levels of soluble scavenger receptors [sCD5 and sCD6] in Sjogren's syndrome patients, either 1ry or 2ry to rheumatoid arthritis [RA] and/or systemic lupus erythematosus [SLE]. Also, to analyze the correlation with clinical and immunological features of Sjogren's syndrome. Twelve consecutive RA patients, seven SLE patients and nine primary Sjogren's syndrome patients were studied. We used a specific enzyme-linked immunosorbent assay [ELISA] to determine sCD5 and sCD6 levels. Immunological tests included antinuclear antibodies [ANA] tested with [indirect immunofluorescence using HEP-2 as the substrate], rheumatoid factor [RF] quantitative [Integra-400- Roche Diagnostics] and complement factors [C3 and C4] [Integra-400- Roche Diagnostics]. We also estimated precipitating antibodies to extractable nuclear antigens Ro/SS-A and La/SS-B autoantibodies with ELISA [Shield Diagnostics]. Detectable levels of sCD5 were found in: 4 [25.7%] RA patients with mean +/- standard error values of 9.4 +/- 4.3 ng/mL; 2 SLE patients [18.2%] with mean +/- standard error values of 8.2 +/- 4.1ng/mL and 4 [41%] primary Sjogren's syndrome patients with mean +/- standard error values of 3.56 +/- 2.9ng/mL. Detectable levels of sCD6 were found in 3 [24.3%] RA patients with mean +/- standard error values of 39.6 +/- 9.61ng/mL; 1 SLE patient [14.3%] with mean +/- standard error values of 33.7 +/- 8.3 ng/mL and 6 [70%] primary Sjogren's syndrome patients with mean +/- standard error values of 26.3 +/- 7.9ng/mL On the other hand, when the CD5 and CD6 levels were compared according to the presence or absence of immunological features [i.e. hypo-complementemia] patients showed higher levels of circulating soluble scavenger receptors [sCD5 and sCD6] [p<0.05 and p<0.01] respectively than those without immunological features. Patients involved in this study showed higher levels of circulating sCD5 and sCD6 when compared with controls. Moreover, the existence of some immunological features [i.e. hypo-complementemia] was associated with high levels of both soluble scavenger receptors