CD28-dependent Rac1 activation is the molecular target of azathioprine in primary human CD4+ T lymphocytes.

By I. Tiede, G. Fritz, Susanne Strand, Daniel Poppe, R. Dvorský, D. Strand, H. Lehr, S. Wirtz, C. Becker, R. Atreya and 10 more. Journal of Clinical Investigation, 2003

822 citations recorded by the source corpus.

Subfields: Genetics, Immunology

View Paper: https://www.semanticscholar.org/paper/62f67da01d1381750403dc0fa88214a7cbbc3680

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. Markus F. Neurath
2. R. Sartor
3. W. Strober
4. J. Turner

In Immunology

1. R. Sartor
2. Markus F. Neurath
3. W. Strober

Citations in the corpus

• Mucosal healing in inflammatory bowel diseases: a systematic review (2012, background): “Several recent studies have addressed the structural consequences of mucosal healing in IBD.”
• Mechanisms of Disease: pathogenesis of Crohn's disease and ulcerative colitis (2006, background): “Several therapies that are effective in the treatment of IBD, including corticosteroids, sulfasalazine, azathioprine, 6-mercaptopurine, infliximab and anti-IL-12 antibody, induce apoptosis of activated T cells and in some cases monocytes”
• Systemic lupus erythematosus: Diagnosis and clinical management. (2019, background): “Besides its antimetabolite role, azathioprine may have a tolerogenic effect by inhibiting CD28-mediated signal 2 in T cells [173].”
• Guidelines for the management of inflammatory bowel disease in adults (2011, background): “Purine antimetabolites inhibit ribonucleotide synthesis, but the mechanism of immunomodulation is by inducing T cell apoptosis by modulating cell (Rac1) signalling.(140) AZA is non-enzymatically metabolised to MP, which involves loss of a nitro-imidazole side chain; this is thought to explain some o”
• The immunological and genetic basis of inflammatory bowel disease (2003, background): “In addition, azathioprine — a commonly used 'conventional' agent in the treatment of Crohn's disease — has recently been shown to function by subverting a co-stimulatory signal into an apoptotic signa”