Chikungunya virus envelope-specific human monoclonal antibodies with broad neutralization potency

10.4049/jimmunol.1003139Journal of Immunology18653258-3264JOIM

Venous thromboembolism prevention in surgery and obstetrics: clinical practice guidelines.

International audienceBACKGROUND AND OBJECTIVE: To produce up-to-date clinical practice guidelines on the prevention of venous thromboembolism in surgery and obstetrics. METHODS: A Steering Committee defined the scope of the topic, the questions to be answered, and the assessment criteria. Eight multidisciplinary working groups (total of 70 experts) performed a critical appraisal of the literature in the following disciplines: pharmacology of antithrombotic agents, orthopaedics; general surgery (gastrointestinal (GI) and varicose vein surgery); urology; gynaecology and obstetrics; thoracic, cardiac and vascular surgery; surgery of the head, neck and spine; and surgery of burns patients. The resultant reports and guidelines were submitted for comment and completion of the Appraisal of Guidelines Research & Evaluation questionnaire to a total of 150 peer reviewers, before producing definite guidelines. RESULTS: The report answers the following questions for each type of surgery: (i) What is the venous thromboembolism incidence according to clinical and/or paraclinical criteria in the absence of prophylaxis? (with stratification of venous thromboembolism risk into low, moderate and high categories); (ii) What is the efficacy and safety of the prophylactic measures used? (iii) When should prophylaxis be introduced and how long should it last? (iv) Does ambulatory surgery affect efficacy and safety of prophylaxis? CONCLUSIONS: Apart from answering the above questions, the guidelines provide a summary table for each discipline. This table stratifies types of surgery into the three risk categories, specifies the recommended prophylaxis for venous thromboembolism (pharmacological and/or mechanical) and grades each recommendation. In addition, whenever appropriate, the recommended prophylaxis is adjusted to low- and high-risk patients

Genomic analysis of Fas and FasL genes and absence of correlation with disease progression in AIDS

Apoptosis has been suggested as a major mechanism for the CD4(+) T-lymphocyte depletion observed in patients infected with human immunodeficiency virus 1 (HIV-1). To evaluate the impact of genetic variations to apoptosis during progression of acquired immunodeficiency syndrome (AIDS), we have performed an extensive genetic analysis of Fas and Fas ligand (FasL) genes. The coding regions and promoters of these genes were resequenced in a cohort of 212 HIV-1-seropositive patients presenting extreme disease phenotypes and 155 healthy controls of Caucasian origin. Overall, 33 single nucleotide polymorphisms (SNPs) with an allele frequency >1% were identified and evaluated for their association with disease progression. Among them, 14 polymorphisms were newly characterized. We did not find any statistically significant association of Fas and FasL polymorphisms and haplotypes with AIDS progression

Immunization against an IL-6 peptide induces anti-IL-6 antibodies and modulates the Delayed-Type Hypersensitivity reaction in cynomolgus monkeys

23581 Madero Dr. Ste. # 101 Mission Viejo, CA 92691interior, prayer hall, view towards qibla wall, 201

Immunogenic, but not steady-state, antigen presentation permits regulatory T-cells to control CD8+T-cell effector differentiation by IL-2 modulation

Absorption of IL-2 is one proposed mechanism of CD4+CD25+FoxP3+ regulatory T cell (Treg) suppression. Direct in vivo experimental evidence for this has recently been obtained. While modulation of IL-2 bioavailability controls CD8+ T-cell effector differentiation under strongly immunogenic conditions it is not known whether Treg modulate CD8+ T cell responses through this mechanism under steady-state conditions. Here we assess this using a mouse model in which dendritic cells (DC) are manipulated to present cognate antigen to CD8+ T cells either in the steady-state or after activation. Our observations show that Treg exert a check on expansion and effector differentiation of CD8+ T cells under strongly immunogenic conditions associated with TLR ligand activation of DC, and this is mediated by limiting IL-2 availability. In contrast, when DC remain unactivated, depletion of Treg has little apparent effect on effector differentiation or IL-2 homeostasis. We conclude that while modulation of IL-2 homeostasis is an important mechanism through which Treg control CD8+ effector differentiation under immunogenic conditions, this mechanism plays little role in modulating CD8+ Tcell differentiation under steady-state conditions