Faculty Opinions recommendation of Posttranscriptional silencing of effector cytokine mRNA underlies the anergic phenotype of self-reactive T cells.

Author(s):  
I-Cheng Ho
Immunity ◽  
2011 ◽  
Vol 34 (1) ◽  
pp. 50-60 ◽  
Author(s):  
Alejandro V. Villarino ◽  
Shoshana D. Katzman ◽  
Eugenio Gallo ◽  
Omer Miller ◽  
Shuwei Jiang ◽  
...  

2010 ◽  
Vol 225 (1-2) ◽  
pp. 167-170 ◽  
Author(s):  
Emilie Jaquiéry ◽  
Samantha Jilek ◽  
Myriam Schluep ◽  
Géraldine Le Goff ◽  
Miguel Garcia ◽  
...  

1993 ◽  
Vol 177 (2) ◽  
pp. 475-482 ◽  
Author(s):  
S R Carding ◽  
W Allan ◽  
A McMickle ◽  
P C Doherty

The patterns of cytokine mRNA expression in mice with primary or secondary influenza pneumonia have been assessed by in situ hybridization analysis of cells from both the mediastinal lymph node (MLN) and the virus-infected lung. Evidence of substantial transcriptional activity was found in all lymphocyte subsets recovered from both anatomical sites. The kinetics of cytokine mRNA expression after primary infection with an H3N2 virus were in accord with the idea that the initial response occurs in regional lymphoid tissue, with the effector T cells later moving to the lung. This temporal separation was much less apparent for the more rapid secondary response resulting from challenge of H3N2-primed mice with an H1N1 virus. Among the T cell receptor alpha/beta+ subsets, transcripts for interferon (IFN) gamma and tumor necrosis factor beta were most commonly found in the CD8+ population whereas mRNA for interleukin (IL) 4 and IL-10 was much more prevalent in CD4+ T cells. The gamma/delta T cells expressed mRNA for all cytokines tested, with IL-2, IL-4, and IFN-gamma predominating among those recovered from the inflammatory exudate. At particular time points, especially early in the MLN and late in the infected lung, the frequency of mRNA+ lymphocytes was much higher than would be expected from current understanding of the prevalence of virus-specific precursors and effectors. If this response is typical, induction of cytokine gene expression for T cells that are not responding directly to the invading pathogen may be a prominent feature of acute virus infections.


Cytokine ◽  
2006 ◽  
Vol 36 (1-2) ◽  
pp. 75-82 ◽  
Author(s):  
Lorella Severino ◽  
Diomira Luongo ◽  
Paolo Bergamo ◽  
Antonia Lucisano ◽  
Mauro Rossi

1993 ◽  
Vol 101 (4) ◽  
pp. 537-542 ◽  
Author(s):  
Hiroyuki Matsue ◽  
Ponciano D Cruz ◽  
Paul R Bergstresser ◽  
Akira Takashima

2007 ◽  
Vol 103 (3) ◽  
pp. 422-428 ◽  
Author(s):  
K. FUJIHASHI ◽  
M. YAMAMOTO ◽  
T. HIROI ◽  
T. V. BAMBERG ◽  
J. R. MCGHEE ◽  
...  

1998 ◽  
Vol 9 (12) ◽  
pp. 2272-2282 ◽  
Author(s):  
M J Penny ◽  
R A Boyd ◽  
B M Hall

The effect of mycophenolate mofetil (MMF) was examined in active Heymann nephritis (HN), an animal model of human membranous nephropathy. HN was induced in Lewis rats with Fx1A/complete Freund's adjuvant (CFA), and controls only received CFA. The induction of HN was prevented by MMF (30 mg/kg per d) from 0 to 4 wk after immunization. Proteinuria was not different in CFA controls up to 16 wk, and was significantly less than in untreated HN from 6 wk onward. Serum anti-Fx1A antibody (Ab) levels and glomerular Ig deposition were suppressed during therapy. The interstitial infiltrate of alphabetaTCR+, CD4+ and CD8+ T cells, natural killer cells, and macrophages (mphi) observed in untreated HN at 8 wk was absent from rats treated from 0 to 4 wk with MMF. Semiquantitative reverse transcription-PCR for renal mononuclear cell cytokine mRNA at 8 wk demonstrated that MMF from 0 to 4 wk prevented the increased expression of Th1 (interferon-gamma, lymphotoxin), Th2 (interleukin-4), and mphi (tumor necrosis factor-alpha) cytokines identified in untreated HN. In lymph node draining sites of immunization, MMF limited both enlargement and the increased proportion of CD3+, CD4+, and CD8+ T cells observed in untreated HN and CFA controls. MMF suppressed Th2 (interleukin-4) but not Th1 (interferon-gamma, lymphotoxin) cytokine mRNA expression in lymph nodes. MMF from 4 to 8, 6 to 12, or 10 to 14 wk did not prevent proteinuria, serum anti-Fx1A Ab, or glomerular IgG deposition when compared with untreated HN. This study showed that MMF from 0 to 4 wk prevented the induction of HN and was associated with preferential suppression of Th2 cytokines. This therapy may prove useful in human idiopathic membranous nephropathy.


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