Example sentences for: interleukin-

How can you use “interleukin-” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • Biological studies have demonstrated increased levels of CD3+/CD25+ lymphocytes [ 5 ] , HTLV-I proviral load and HTLV-I tax/rex mRNA expression [ 6 7 ] , HTLV-I specific IgA [ 8 ] , soluble interleukin-2 receptors [ 9 ] , beta-chemokines [ 7 ] and soluble intracellular adhesion molecule-1 (ICAM-1) [ 10 ] , in bronchoalveolar lavage fluid from HTLV-I infected humans.

  • In particular, even a low level of viremia correlates with a low or undetectable frequency of interleukin-2-producing HIV-1-specific memory CD4+ T cells endowed with proliferative capacity in vitro [36,37,38,39], thus abrogating CD4+ T cell help crucial to maintain efficacy of CD8+ T cell functions.

  • Other investigators described differences of the same order of magnitude between mouse strains in expression of transgenes encoding α1-antitrypsin [ 1 ] , interleukin-12 [ 2 ] , and human endostatin [ 3 ] . These differences in transgene expression between inbred species may have clinical implications, as differences between inbred strains are considered to reflect differences between individuals of an outbred species.

  • The transcription factors NF-κB and CREB have been reported to activate COX-2 in LPS-stimulated monocytes and macrophages in vitro [ 48 49 ] . Moreover, endotoxin-induced increases in neutrophil TNF-α, as well as interleukin-1β and MIP-2 in vivo appear to be mediated by NF-κB and CREB [ 21 ] . We found that activated NF-κB and CREB were present in the nucleus of adherent vascular lung neutrophils from endotoxemic, but not control rats, suggesting that these transcription factors play a role in increased responsiveness of the cells.

  • Once in the tissue, monocytes undergo the poorly understood process of transformation to macrophages with altered morphology and function [ 19 ] . In arthritis, synovial macrophages might cause joint destruction by differentiating to bone-resorbing osteoclasts [ 20 ] or by releasing cartilage-degrading enzymes and cytokines, such as interleukin-1 and tumor necrosis factor-α [ 8 ] . It has therefore been suggested that therapies for chronic arthritis should be aimed at depleting joint mononuclear cells or controlling the activation of synovial macrophages [ 21 ] . Indeed, elimination of macrophages by clodronate-laden liposomes in rat models of adjuvant [ 22 ] and antigen-induced arthritis [ 23 ] induces amelioration of the arthritis.


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