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Stolina M Bolon B Middleton S Dwyer D Brown H Duryea D Zhu L Rohner A Pretorius J Kostenuik P Feige U Zack D 《Journal of clinical immunology》2009,29(2):158-174
Introduction Rats with adjuvant-induced arthritis (AIA) were necropsied on 14 occasions during preclinical, acute clinical and chronic
clinical stages of AIA progression to characterize local (joint protein extracts) and systemic (serum) levels of mediators
regulating inflammation and bone erosion in conjunction with lymphoid tissue-specific leukocyte kinetics.
Results Systemic increases in alpha1 acid glycoprotein, tumor necrosis factor-α (TNFα), interleukin (IL)-17, transforming growth factor
beta (TGFβ), and chemokine (C–C motif) ligand 2 (CCL2) together with local IL-1α/β and TGFβ enrichment and local lymphoid
hyperplasia preceded the onset of clinical disease and joint damage. Systemic upregulation of TNFα, IL-6, IL-17, TGFβ, IL-18,
CCL2, receptor activator of nuclear factor-κβ ligand (RANKL), and prostaglandin E2 during acute and/or chronic AIA coincided with systemic leukocytosis and CD4+ T cell increase in blood and spleen. In contrast,
progression of joint erosions during clinical AIA was associated with intra-articular increases in IL-1α/β, IL-6, RANKL, IL-17,
TGFβ, CCL2, and KC/GRO and also a dramatic decline in osteoprotegerin.
Conclusion These data indicate that systemic and local events in inflammatory arthritis are discrete processes, driven by multiple cellular
and humoral mediators with distinct kinetic profiles. 相似文献
996.
Julie M. Decker Kenneth P. Zammit Juliet L. Easlick Mario L. Santiago Denise Bonenberger Beatrice H. Hahn Olaf Kutsch Frederic Bibollet-Ruche 《Virology》2009,394(1):109-118
Human immunodeficiency virus type 1 (HIV-1) originated in chimpanzees; yet, several previous studies have shown that primary HIV-1 isolates replicate poorly in chimpanzee CD4+ T lymphocytes in vitro and in vivo. The reasons for this apparent restriction are not understood. Here, we describe a new activation protocol that led to a reproducible expansion and activation of chimpanzee CD4+ T lymphocytes in vitro. Using this protocol, we uncovered species-specific differences in the activation profiles of human and chimpanzee CD4+ T-cells, including HLA-DR and CD62L. Moreover, we found that improved activation facilitated the replication of both CXCR4 and CCR5-tropic HIV-1 in CD4+ T-cell cultures from over 30 different chimpanzees. Thus, the previously reported “replication block” of CCR5-tropic HIV-1 in chimpanzee lymphocytes appears to be due, at least in large part, to suboptimal T-cell activation. 相似文献
997.
Naturally acquired immunity to falciparum malaria protects millions of people routinely exposed to Plasmodium falciparum infection from severe disease and death. There is no clear concept about how this protection works. There is no general agreement about the rate of onset of acquired immunity or what constitutes the key determinants of protection; much less is there a consensus regarding the mechanism(s) of protection. This review summarizes what is understood about naturally acquired and experimentally induced immunity against malaria with the help of evolving insights provided by biotechnology and places these insights in the context of historical, clinical, and epidemiological observations. We advocate that naturally acquired immunity should be appreciated as being virtually 100% effective against severe disease and death among heavily exposed adults. Even the immunity that occurs in exposed infants may exceed 90% effectiveness. The induction of an adult-like immune status among high-risk infants in sub-Saharan Africa would greatly diminish disease and death caused by P. falciparum. The mechanism of naturally acquired immunity that occurs among adults living in areas of hyper- to holoendemicity should be understood with a view toward duplicating such protection in infants and young children in areas of endemicity. 相似文献
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Feng Li Emily C. Lisi Elizabeth S. Wohler Ada Hamosh Denise A.S. Batista 《European journal of medical genetics》2009,52(5):349-352
An inherited, interstitial subtelomere deletion of approximately 1.3–1.4 Mb at 3q29 was identified in a patient and his father utilizing BAC array comparative genomic hybridization (a-CGH). The imbalance was located within the common 3q29 microdeletion syndrome region and shared the distal breakpoint with prior published cases. However, our patient was developmentally normal at 6 months of age and his father is a functional adult, who had mild developmental delay in childhood. They presented with congenital cardiac defects including patent ductus arteriosus. In addition, the patient had subvalvular aortic stenosis and his father had pulmonic stenosis. These defects were not present in most of the previously reported 3q29 microdeletion cases. This case expands the phenotypic findings associated with 3q29 microdeletion syndrome, suggesting an association with cardiac defect. It also raises the possibility of normal cognition in adulthood. 相似文献
1000.
Denise Salles Coelho da Mota Eliane Furtado Daniel Alexandre Bottino Eliete Bouskela 《Clinics (S?o Paulo, Brazil)》2009,64(8):797-802