31 research outputs found
GENETIC DIVERGENCE AND MORPHO-AGRONOMIC PERFORMANCE OF JATROPHA CURCAS L. CLONES FOR SELECTION OF CLONAL VARIETIES
Aberrant Expression of Functional BAFF-System Receptors by Malignant B-Cell Precursors Impacts Leukemia Cell Survival
Despite exhibiting oncogenic events, patient's leukemia cells are responsive and dependent on signals from their malignant bone marrow (BM) microenvironment, which modulate their survival, cell cycle progression, trafficking and resistance to chemotherapy. Identification of the signaling pathways mediating this leukemia/microenvironment interplay is critical for the development of novel molecular targeted therapies
Cracking the BAFF code.
The tumour necrosis factor (TNF) family members B cell activating factor (BAFF) and APRIL (a proliferation-inducing ligand) are crucial survival factors for peripheral B cells. An excess of BAFF leads to the development of autoimmune disorders in animal models, and high levels of BAFF have been detected in the serum of patients with various autoimmune conditions. In this Review, we consider the possibility that in mice autoimmunity induced by BAFF is linked to T cell-independent B cell activation rather than to a severe breakdown of B cell tolerance. We also outline the mechanisms of BAFF signalling, the impact of ligand oligomerization on receptor activation and the progress of BAFF-depleting agents in the clinical setting
PED-BD cohort 2013: expert consensus classification gives higher sensitivity than the international study group criteria to define Behcet’s disease in children
PED-BD COHORT 2013: EXPERT CONSENSUS CLASSIFICATION GIVES HIGHER SENSITIVITY THAN THE INTERNATIONAL STUDY GROUP CRITERIA TO DEFINE BEHCET'S DISEASE IN CHILDREN
PED-BD, COHORT STUDY FOR PAEDIATRIC BEHCET'S DISEASE: UPDATE 2012 REPORTING 206 PATIENTS
Pres-Final-2319: Ped-Bd Cohort 2013: Expert Consensus Classification Gives Higher Sensitivity Than The International Study Group Criteria To Define Behcet'S Disease In Children
PubMe
Treatment of autoinflammatory diseases: results from the Eurofever Registry and a literature review
To evaluate the response to treatment of autoinflammatory diseases from an international registry and an up-to-date literature review
Defining the transcriptional and cellular landscape of type 1 diabetes in the NOD mouse.
Our ability to successfully intervene in disease processes is dependent on definitive diagnosis. In the case of autoimmune disease, this is particularly challenging because progression of disease is lengthy and multifactorial. Here we show the first chronological compendium of transcriptional and cellular signatures of diabetes in the non-obese diabetic mouse. Our data relates the immunological environment of the islets of Langerhans with the transcriptional profile at discrete times. Based on these data, we have parsed diabetes into several discrete phases. First, there is a type I interferon signature that precedes T cell activation. Second, there is synchronous infiltration of all immunological cellular subsets and a period of control. Finally, there is the killing phase of the diabetogenic process that is correlated with an NF-kB signature. Our data provides a framework for future examination of autoimmune diabetes and its disease progression markers