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《实验药学杂志》2006年第05期

mif magnifies malarial anemia
loose lipid rafts lead to trigger-happy mast cells
celiac ctls change their stripes
platelets pull in progenitors
transforming with telomerase
ignoring endotoxin
singapore's multibillion dollar gamble
telomerase flies the coop: the telomerase rna component as a viral-encoded oncogene
bax does not have to adopt its final form to drive t cell death
plasmacytoid dendritic cells inhibit pulmonary immunopathology and promote clearance of respiratory syncytial virus
cholesterol deficiency in a mouse model of smith-lemli-opitz syndrome reveals increased mast cell responsiveness
fas-positive t cells regulate the resolution of airway inflammation in a murine model of asthma
a critical role for the host mediator macrophage migration inhibitory factor in the pathogenesis of malarial anemia
mechanisms imposing the v? bias of v14 natural killer t cells and consequences for microbial glycolipid recognition
nod.c3c4 congenic mice develop autoimmune biliary disease that serologically and pathogenetically models human primary biliary cirrhosis
platelets secrete stromal cell
human mesenchymal stem cells exert potent antitumorigenic effects in a model of kaposi's sarcoma
toll-like receptor agonists influence the magnitude and quality of memory t cell responses after prime-boost immunization in nonhuman primates
radiation modulates the peptide repertoire, enhances mhc class i expression, and induces successful antitumor immunotherapy
lymphocyte recruitment into the aortic wall before and during development of atherosclerosis is partially l-selectin dependent
rar is critical for maintaining a balance between hematopoietic stem cell self-renewal and differentiation
the c-flip
the impact of dm on mhc class ii
e proteins and notch signaling cooperate to promote t cell lineage specification and commitment
a virus-encoded telomerase rna promotes malignant t cell lymphomagenesis
reprogramming of ctls into natural killer
maintenance of viral suppression in hiv-1
protective immune responses against west nile virus are primed by distinct complement activation pathways
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