Cytokines and Chemokine Gene Expression in Human Kidney Transplantation

Hřibová, Petra; Kotsch, Katja; Brabcova, Irena; Vı́tko, Štefan; Volk, Hans‐Dieter; Lácha, J

doi:10.1016/j.transproceed.2004.12.177

Cited by 30 publications

(28 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ubiquitously expressed NFI may facilitate the low-level replication of persistent BKV in kidney epithelial cells by increasing the level (and activity) of Pol-primase at the core-ori. Also, signaling mediated through TGF-␤ (3, 4), tumor necrosis factor alpha (TNF-␣) (4), and oxidative stress (5,(56)(57)(58) induced by kidney ischemia/reperfusion injury and/or inflammatory responses (12,23,38) during kidney transplantation or by the administration of immunosuppressive drugs such as tacrolimus and cyclosporine (67) might alter NFI isotype expression or activity and thereby promote the NFI-mediated recruitment of Tag and/or Polprimase to the viral core-ori. These notions can be tested experimentally.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of BK Virus DNA Replication by NFI Family Transcription Factors

Liang

Tikhanovich

Nasheuer

et al. 2012

J Virol

View full text Add to dashboard Cite

b BK polyomavirus (BKV) establishes persistent, low-level, and asymptomatic infections in most humans and causes polyomavirus-associated nephropathy (PVAN) and other pathologies in some individuals. The activation of BKV replication following kidney transplantation, leading to viruria, viremia, and, ultimately, PVAN, is associated with immune suppression as well as inflammation and stress from ischemia-reperfusion injury of the allograft, but the stimuli and molecular mechanisms leading to these pathologies are not well defined. The replication of BKV DNA in cell cultures is regulated by the viral noncoding control region (NCCR) comprising the core origin and flanking sequences, to which BKV T antigen (Tag), cellular proteins, and small regulatory RNAs bind. Six nuclear factor I (NFI) binding sites occur in sequences flanking the late side of the core origin (the enhancer) of the archetype virus, and their mutation, either individually or in toto, reduces BKV DNA replication when placed in competition with templates containing intact BKV NCCRs. NFI family members interacted with the helicase domain of BKV Tag in pulldown assays, suggesting that NFI helps recruit Tag to the viral core origin and may modulate its function. However, Tag may not be the sole target of the replication-modulatory activities of NFI: the NFIC/CTF1 isotype stimulates BKV template replication in vitro at low concentrations of DNA polymerase-␣ primase (Pol-primase), and the p58 subunit of Polprimase associates with NFIC/CTF1, suggesting that NFI also recruits Pol-primase to the NCCR. These results suggest that NFI proteins (and the signaling pathways that target them) activate BKV replication and contribute to the consequent pathologies caused by acute infection.

show abstract

Section: Discussionmentioning

confidence: 99%

Stimulation of BK Virus DNA Replication by NFI Family Transcription Factors

Liang

Tikhanovich

Nasheuer

et al. 2012

J Virol

View full text Add to dashboard Cite

show abstract

“…39,40 Initially approved by the FDA for use in treating Crohn disease, infliximab has since been approved for use in ulcerative colitis, rheumatoid arthritis, ankylosing spondylitis and plaque psoriasis. After serum TNF levels were shown to be significantly elevated during acute rejection episodes in kidney transplant patients relative to non-rejecting controls, 41 infliximab has been used as an off-label induction agent in several recent pilots. There is great interest in the forthcoming results of these studies, especially in light of contrary evidence from Karczerski et al stating that TNF levels are not significantly elevated during acute rejection episodes in kidney allograft recipients.…”

Section: Anti-b-cell Therapiesmentioning

confidence: 99%

“…There is great interest in the forthcoming results of these studies, especially in light of contrary evidence from Karczerski et al stating that TNF levels are not significantly elevated during acute rejection episodes in kidney allograft recipients. 41 This would suggest a TNF-independent rejection mechanism, one that infliximab would be unlikely to counteract.…”

Section: Anti-b-cell Therapiesmentioning

confidence: 99%

Antibody immunosuppressive therapy in solid organ transplant

Klipa

Mahmud

Ahsan

2010

mAbs

View full text Add to dashboard Cite

“…Proinflammatory cytokines of the interleukin (IL) [20,21], interferon (IFN) [22]tumor necrosis factor (TNF) [23], growth factor [24][25][26][27][28][29] and chemokine families have been shown to play a role in tissue damage and vascular remodeling during inflammation [30][31][32][33][34], in renal injury and repair [35], idiopathic membranous nephropathy [36], glomerulonephritis and allograft rejection during transplantation [37,38]. Concise reviews of the chemokine/cytokine cocktail and their role in inflammation and fibrosis in different organs is available elsewhere [38][39][40].…”

Section: Inflammation and The Role Of Cytokines Growth Factors And Cmentioning

confidence: 99%

Fibrosis, chronic inflammation and new pathways for drug discovery

Sivakumar¹,

Das²

2008

Inflamm. res.

View full text Add to dashboard Cite

Recent studies have challenged the conventional hypothesis that inflammation is the major player in the fibrosis cascade. Emerging evidence points to a critical role for interactions between tissue-resident and infiltrating, non-resident cells, in mediating fibrotic responses. Improved understanding of the biology of extracellular matrix (ECM) remodeling and the pathways that regulate assembly of the ECM and its interactions with growth factors/cytokines have led to the identification of new and attractive therapeutic targets. These include molecules that regulate fibrocytic cell infiltration, epithelial and myofibroblast differentiation, ECM synthesis and degradation. However, it is imperative that these new therapies be timed and compartmentalized to target the tissue of interest, as the dynamics of cellular differentiation and ECM remodeling may be different between organ systems. This review will summarize the current understanding of the mechanisms involved in the development of fibrosis, based on recent in vitro and in vivo studies, and comment on novel molecular pathways for drug discovery.

show abstract

Cytokines and Chemokine Gene Expression in Human Kidney Transplantation

Cited by 30 publications

References 12 publications

Stimulation of BK Virus DNA Replication by NFI Family Transcription Factors

Stimulation of BK Virus DNA Replication by NFI Family Transcription Factors

Antibody immunosuppressive therapy in solid organ transplant

Fibrosis, chronic inflammation and new pathways for drug discovery

Contact Info

Product

Resources

About