Stefan Höxtermann

Mechanisms of apoptosis: UVA1‐induced immediate and UVB‐induced delayed apoptosis in human T cells in vitro†

Objective The decreased number of lymphocytes combined with the induction of apoptosis and necrosis seems to be the key mechanism of many phototherapeutic agents. The purpose of our study was to determine the regulating pathway, time course and dose dependence of UVA1‐ vs. UVB‐induced cell death in human T lymphocytes.

Increased serum IL-33 levels may indicate vascular involvement in systemic sclerosis

Interleukin 33 (IL-33) belongs to the IL-1 family and was found in smooth muscle cells, epithelial cells, fibroblasts, keratinocytes, endothelial cells, dendritic cells and activated macrophages.1 IL-33 binds the orphan receptor ST2 and induces gene expression of Th2-associated cytokines. Treatment of wild-type mice with IL-33 led to changes in vessels, digestive tract and lungs.2 Manetti et al 3 recently investigated serum IL-33 levels by means of an ELISA in 58 patients with systemic sclerosis (SSc) and 30 healthy individuals. They observed that serum IL-33 was significantly increased in patients with SSc as compared with healthy controls. They also found that serum IL-33 levels were associated with early disease stage and microvascular involvement as determined by capillaroscopy. The study of Manetti et al 3 prompted us to investigate serum IL-33 …

Neurological disorders in patients with bullous pemphigoid: clinical and experimental investigations.

Previous studies have shown that patients with bullous pemphigoid (BP) are more likely to have neurological diseases (ND).

Glutathione-S-transferase T1 genotyping and phenotyping in psoriasis patients receiving treatment with oral fumaric acid esters.

Glutathione S‐transferases (GSTs) are involved in detoxification of xenobiotics such as fumaric acid esters (FAE).

Occurrence of circulating anti-bullous pemphigoid antibodies in patients with lichen sclerosus.

References 1 Drago F, Broccolo F, Rebora A. Pityriasis rosea: an update with a critical appraisal of its possible herpesviral etiology. J Am Acad Dermatol 2009; 61: 303–318. 2 Hudson LD, Adelman S, Lewis CW. Pityriasis rosea. Viral complement fixation studies. J Am Acad Dermatol 1981; 4: 544–546. 3 Laguna-Torres VA, Benavides JG. Infection and death from influenza A H1N1 virus in Mexico. Lancet 2009; 374: 2032–2033. 4 Gonzalez BE, Brust DG. Novel influenza A (H1N1) presenting as an acute febrile encephalopathy in a mother and daughter. Clin Infect Dis 2009; 49: 1966–1967. 5 Cao B, Li XW, Mao Y et al. Clinical features of the initial cases of 2009 pandemic influenza A (H1N1) virus infection in China. N Engl J Med 2009; 361: 2507–2517.

Detection of clonal T cells in the circulation of patients with nephrogenic systemic fibrosis.

BACKGROUND Nephrogenic systemic fibrosis is a sclerodermalike disease in patients with acute or chronic renal insuffiency related to administration of gadolinium-containing contrast agents. Previous studies have demonstrated clonal T-cell populations in the blood of patients with systemic sclerosis, suggesting that these cells may be involved in the pathogenesis of the disease. Facing the clinical similarities of both diseases, we hypothesized that clonal expansion of T cells could be present in nephrogenic systemic fibrosis as well. OBSERVATIONS Findings from polymerase chain reaction and high-resolution capillary electrophoresis for T-cell receptor gamma gene rearrangement analysis showed that all 6 prospectively evaluated patients (100%) with nephrogenic systemic fibrosis had detectable clonal T cells in their peripheral blood. In contrast, only 4 of the 15 control patients (27%) with chronic renal failure and none of the 12 healthy individuals analyzed in this study had evidence for T-cell clonality using the same type of examination. Clonal T-cell-positive patients with systemic sclerosis have previously been reported to better respond to extracorporeal photopheresis. However, this was not the case in 2 of our patients with nephrogenic systemic fibrosis. Conclusion As in systemic sclerosis, clonally expanded T-cell populations could play a critical role in the pathogenesis of nephrogenic systemic fibrosis, probably as an in vivo-activated inflammatory response to gadolinium exposure.

Severe dyslipidemia and immune activation in HIV patients with dysglycemia.

Background and Objective: Diabetes mellitus (DM) is common in human immunodeficiency virus (HIV)-infected patients. However, the relationship between dysglycemia, lipid metabolism, and immune activation in HIV patients is poorly understood. Methods: We retrospectively analyzed the clinical data of 180 HIV patients, including 153 patients undergoing highly active antiretroviral therapy (HAART) and 27 HAART-naive patients. DM was defined as fasting serum glucose levels ≥126 mg/dl, and impaired fasting glucose (IFG) was defined as serum glucose levels of 101–125 mg/dl at two different time points. Lipid metabolic indexes were measured. CD4+, CD8+, and CD8+ HLA-DR+ T cells were determined by flow cytometry. Results: IFM and DM percentages were higher in the HAART group than in the HAART-naive group (59.5% vs. 48.1% and 21.6% vs. 7.4%, respectively; p < 0.01). Additionally, DM percentage was high in patients receiving HAART containing protease inhibitors. Serum levels of triglycerides and very low-density lipoprotein cholesterol were higher in IFG and DM HAART patients than in euglycemic HAART patients (p < 0.05). Serum triglyceride levels were higher in HAART-naive DM patients than in other patients (p < 0.05). CD8+ and CD8+ HLA-DR+ cell counts were higher in IFG and DM HAART patients than in euglycemic HAART patients (p < 0.05). Ordinal logistic regression analysis suggested that TRIG, VLDL, CD8, and HAART were predictors of glucose metabolic disorders. Conclusion: HIV patients with hyperglycemia have severe dyslipidemia and immune activation, and HAART is an important impact factor of glucose and lipid metabolic disorders.

Prevalence and Influencing Factors of Thyroid Dysfunction in HIV-Infected Patients

Thyroid dysfunction is more common in human immunodeficiency virus (HIV) patients. But the effects of highly active antiretroviral therapy (HAART) and hepatitis B/C virus (HBV/HCV) coinfection on thyroid function is unclear. We retrospectively reviewed the data of 178 HIV patients and determined the prevalence of thyroid dysfunction and the relationship between thyroid hormone levels, CD4 cell count, HIV-1 duration, HAART duration/regimens, and HBV/HCV coinfection. Of the 178 patients, 59 (33.1%) had thyroid dysfunction, mostly hypothyroidism. Thyroid dysfunction was significantly more frequent in the HAART group (41/104, 39.4%) than in the HAART-naïve group (18/74, 24.3%; P < 0.05). The mean CD4 cell count was significantly lower in patients with hypothyroidism (372 ± 331/μL) than in the other patients (P < 0.05). The FT4 level was significantly lower in the HAART group than in the HAART-naïve group (1.09 ± 0.23 versus 1.20 ± 0.29 pg/mL, P < 0.05). FT3/FT4 levels were negatively related to HIV duration and FT3 levels were positively related to CD4 cell (P < 0.05). HBV patients had lower FT3 levels, while HCV patients had higher FT3 and FT4 levels (P < 0.05). Thyroid dysfunction is more common in HIV patients on HAART, mainly manifested as hypothyroidism. FT3/FT4 levels are correlated with HIV progression. HBV/HCV coinfection increases the probability of thyroid dysfunction.

Flowzytometrische Messung der Aktivierung basophiler Granulozyten in der Diagnostik der Wespengiftallergie

Die Diagnose der Insektengiftallergie basiert auf Anamnese, Nachweis von spezifischem IgE und Hauttest [7],[8]. Andere Verfahren wie Histaminfreisetzungs-test (HFT), Basophilendegranulationstest (BDT), Immunoblot oder Sulfidoleukotrienstimulation zahlen derzeit nicht zu den Routineverfahren, konnen jedoch in Einzelfallen zusatzliche Informationen liefern [1],[4],[5],[7],[13].

MicroRNA‐155 is a biomarker of T‐cell activation and immune dysfunction in HIV‐1‐infected patients

MicroRNA‐155 (miR‐155) regulates T‐cell differentiation and activation. It has also been associated with HIV infection. However, it remains unclear whether miR‐155 is related to the T‐cell response in HIV‐infected individuals (e.g. T‐cell activation and exhaustion).