scholarly journals Whole blood interleukin‐2 release test to detect and characterise rare circulating gluten‐specific t cell responses in coeliac disease

Author(s):  
Robert P Anderson ◽  
Gautam Goel ◽  
Melinda Y. Hardy ◽  
Amy K. Russell ◽  
Suyue Wang ◽  
...  
Methods ◽  
2006 ◽  
Vol 38 (2) ◽  
pp. 77-83 ◽  
Author(s):  
Tanja Breinig ◽  
Martina Sester ◽  
Urban Sester ◽  
Andreas Meyerhans

2011 ◽  
Vol 365 (22) ◽  
pp. 2067-2077 ◽  
Author(s):  
David Saadoun ◽  
Michelle Rosenzwajg ◽  
Florence Joly ◽  
Adrien Six ◽  
Fabrice Carrat ◽  
...  

2010 ◽  
Vol 84 (20) ◽  
pp. 10923-10927 ◽  
Author(s):  
Michael Molloy ◽  
Weijun Zhang ◽  
Edward Usherwood

ABSTRACT Interleukin-2 (IL-2) has been implicated as being necessary for the optimal formation of primary CD8+ T cell responses against various pathogens. Here we have examined the role that IL-2 signaling plays in several aspects of a CD8+ T cell response against murine gammaherpesvirus 68 (MHV-68). Exposure to MHV-68 causes a persistent infection, along with infectious mononucleosis, providing a model for studying these processes in mice. Our study indicates that CD25 is necessary for optimal expansion of the antigen-specific CD8+ T cell response but not for the long-term memory response. Contrastingly, IL-2 signaling through CD25 is absolutely required for CD8+ T cell mononucleosis.


PLoS Medicine ◽  
2016 ◽  
Vol 13 (10) ◽  
pp. e1002139 ◽  
Author(s):  
John A. Todd ◽  
Marina Evangelou ◽  
Antony J. Cutler ◽  
Marcin L. Pekalski ◽  
Neil M. Walker ◽  
...  

2005 ◽  
Vol 142 (2) ◽  
pp. 333-340 ◽  
Author(s):  
M. Raki ◽  
O. Molberg ◽  
S. Tollefsen ◽  
K. E. A. Lundin ◽  
L. M. Sollid

2001 ◽  
Vol 155 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Yoichiro Kusunoki ◽  
Tomonori Hayashi ◽  
Yukari Morishita ◽  
Mika Yamaoka ◽  
Mayumi Maki ◽  
...  

2012 ◽  
Vol 80 (5) ◽  
pp. 1744-1752 ◽  
Author(s):  
Katrine M. Jensen ◽  
Jesper Melchjorsen ◽  
Frederik Dagnaes-Hansen ◽  
Uffe B. S. Sørensen ◽  
Rune R. Laursen ◽  
...  

ABSTRACTSynthetic oligodeoxynucleotides (ODN) containing unmethylated CpG motifs, CpG ODN, are Toll-like receptor 9 agonists (TLR9a), which have been used as adjuvants in pneumococcal vaccines to improve antibody responses in immunodeficient patients. Here, we examined whether the coadministration of TLR9a with pneumococcal CRM197-conjugate vaccine enhances protection against pneumococcal colonization, the levels of antipolysaccharide antibodies, and the CD4+T-cell responses. Wild-type BALB/c mice and B-cell-deficient BALB/c Igh-Jtm1Dhumice were immunized twice with the following: (i) PCV alone; (ii) simultaneous PCV and TLR9a; (iii) PCV and then TLR9a, after a 48-h delay; (iv) TLR9a alone; and (v) phosphate-buffered saline. Nasopharyngeal protection, serum antibodies, CD4+T-cell responses, and clearance of bacteremia after intraperitoneal challenge withStreptococcus pneumoniae6B were evaluated. We found decreased nasopharyngeal protection againstS. pneumoniae6B colonization after simultaneous immunization with PCV and TLR9a compared to immunization with PCV alone in wild-type BALB/c mice (P= 0.037). A similar trend was observed in B-cell-deficient BALB/c Igh-Jtm1Dhumice. Simultaneous administration did not enhance antibody levels and lowered the CRM197-specific cytokine release of gamma interferon, interleukin-2 (IL-2), IL-5 and IL-13. Immunization with PCV and then TLR9a, after a 48-h delay, significantly improved nasopharyngeal protection compared to simultaneous administration (P= 0.011). Furthermore, delaying TLR9a delivery increased antibody titers compared to both simultaneous administration (P= 0.001) and PCV immunization alone (P= 0.026). In conclusion, the immunological and clinical impact of adjuvanting a pneumococcal conjugate vaccine (Prevnar; Pfizer) with a TLR9a is highly depended on timing of the adjuvant administration. Thus, careful timing of adjuvant administration may improve novel vaccine formulations.


2008 ◽  
Vol 82 (19) ◽  
pp. 9629-9638 ◽  
Author(s):  
Monica Vaccari ◽  
Joseph Mattapallil ◽  
Kaimei Song ◽  
Wen-Po Tsai ◽  
Anna Hryniewicz ◽  
...  

ABSTRACT Adaptive CD4+ and CD8+ T-cell responses have been associated with control of human immunodeficiency virus/simian immunodeficiency virus (HIV/SIV) replication. Here, we have designed a study with Indian rhesus macaques to more directly assess the role of CD8 SIV-specific responses in control of viral replication. Macaques were immunized with a DNA prime-modified vaccinia virus Ankara (MVA)-SIV boost regimen under normal conditions or under conditions of antibody-induced CD4+ T-cell deficiency. Depletion of CD4+ cells was performed in the immunized macaques at the peak of SIV-specific CD4+ T-cell responses following the DNA prime dose. A group of naïve macaques was also treated with the anti-CD4 depleting antibody as a control, and an additional group of macaques immunized under normal conditions was depleted of CD8+ T cells prior to challenge exposure to SIVmac251. Analysis of the quality and quantity of vaccine-induced CD8+ T cells demonstrated that SIV-specific CD8+ T cells generated under conditions of CD4+ T-cell deficiency expressed low levels of Bcl-2 and interleukin-2 (IL-2), and plasma virus levels increased over time. Depletion of CD8+ T cells prior to challenge exposure abrogated vaccine-induced protection as previously shown. These data support the notion that adaptive CD4+ T cells are critical for the generation of effective CD8+ T-cell responses to SIV that, in turn, contribute to protection from AIDS. Importantly, they also suggest that long-term protection from disease will be afforded only by T-cell vaccines for HIV that provide a balanced induction of CD4+ and CD8+ T-cell responses and protect against early depletion of CD4+ T cells postinfection.


2003 ◽  
Vol 71 (4) ◽  
pp. 1755-1762 ◽  
Author(s):  
Anna Lundgren ◽  
Elisabeth Suri-Payer ◽  
Karin Enarsson ◽  
Ann-Mari Svennerholm ◽  
B. Samuel Lundin

ABSTRACT Helicobacter pylori colonizes the gastric and duodenal mucosa. The infection normally persists for life and causes peptic ulcers and gastric cancer in a subset of infected individuals. We hypothesized that the inability to clear the infection may be a consequence of H. pylori-specific regulatory T cells that actively suppress T-cell responses. Therefore, we characterized the T-cell responses to H. pylori in H. pylori-infected individuals without any subjective symptoms and in uninfected control subjects and investigated the role of regulatory CD4+ CD25high T cells during infection. The stimulation of CD4+ peripheral blood T cells with monocyte-derived dendritic cells pulsed with a membrane preparation of H. pylori resulted in proliferation and gamma interferon production in both infected and uninfected individuals. Sorted memory cells from infected individuals responded less than cells from uninfected subjects, and the unresponsiveness could be abolished by depletion of CD4+ CD25high regulatory T cells or the addition of interleukin 2. Furthermore, CD4+ CD25high T cells suppressed H. pylori-induced responses in cocultures with CD25low/− cells. Tetanus toxoid induced comparable responses in memory cells from infected and uninfected individuals in both the presence and the absence of regulatory T cells, suggesting that the suppression was H. pylori specific. In conclusion, we have shown that H. pylori-infected individuals have impaired memory CD4+ T-cell responses to H. pylori that are linked to the presence of H. pylori-specific regulatory T cells that actively suppress the responses.


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