scholarly journals Innate memory phenotype CD4+ T cells play a role in early protection against infection by Listeria monocytogenes in a CD30L-dependent manner

2011 ◽  
Vol 55 (9) ◽  
pp. 645-656 ◽  
Author(s):  
Kenji Umeda ◽  
Xun Sun ◽  
Ying Guo ◽  
Hisakata Yamada ◽  
Kensuke Shibata ◽  
...  
2019 ◽  
Vol 12 (10) ◽  
pp. 1529-1534
Author(s):  
Linda Haryadi ◽  
Eddy Suprayitno ◽  
Aulanni'am Aulanni'am ◽  
Anik Martinah Hariati

Background and Aim: Anisakis is a global challenge for a fish product which may lead to a decrease in economic value and consumers' preference. Skipjack (Katsuwonus pelamis) in Kupang, Nusa Tenggara Timur, Indonesia, have important economic value for local fisheries. Anisakis typica is one of the Anisakis species which potent to induce an allergic reaction. However, the study about A. typica involved in the dendritic cells (DCs), T helper 1 (Th1), T helper 2 (Th2), and regulatory T cells (Tregs) is still limited. This study aimed to analyze the dynamic changed of the immune system including DCs, CD4+ T cells, and Tregs after 1 week of A. typica sensitization. Materials and Methods: Twenty-four male Balb/C mice were randomly divided into four groups (n=6), mice treated with crude A. typica extract (CAE) 50, 75, and 100 mg/kg BW, respectively. CAE was given orally per day for a week. At the end of the experiment, the animals were sacrificed and the spleen was collected. DCs were labeled as CD11c+ interleukin-6+ (IL-6+); CD4+ T cells were distinguished as Th1 (CD4+ interferon-γ+ [IFN-γ+]) and Th2 (CD4+ IL-4+ and CD4+ IL-5+); Tregs were labeled as CD4+CD25+CD62L+. The expression of each cell was determined by flow cytometry. Results: Our result described that CAE elicits CD11c+ IL-6+, CD4+ IFN-γ+, CD4+ IL-4+, and CD4+ IL-5+ and reduces CD4+CD25+CD62L+ significantly (p<0.05) in dose-dependent manner in mice after A. typica infection. Conclusion: The Th1/Th2 ratio after A. typica crude extract treatment exhibits a mixed pattern rather than the classical model allergy to food antigens. Our study is expected as a basic understanding of the changes in immune response after A. typica infection.


2015 ◽  
Vol 36 (1) ◽  
pp. 133-140 ◽  
Author(s):  
Jin-Chao Xu ◽  
Yong-Bo Peng ◽  
Ming-Yu Wei ◽  
Yi-Fan Wu ◽  
Donglin Guo ◽  
...  

Background/Aims: Bitter-tasting chloroquine can suppress T cell activation by inhibiting Ca2+ signaling. However, the mechanism of inhibition remains largely unclear. Methods: In this study, CD4+ T cells were isolated from the thymus, and the calcium content of CD4+ thymocytes was measured using fura-2 AM and a TILL imaging system. Pyrazole-3 (Pyr3), thapsigargin (TG), and caffeine were used to assess the effects of chloroquine on the intracellular Ca2+ content of CD4+ T cells. Results: In murine CD4+ thymocytes, chloroquine decreased the TG-triggered intracellular Ca2+ increase in a dose-dependent manner. In the absence of chloroquine under Ca2+-free conditions (0 mM Ca2+ and 0.5 mM EGTA), TG induced a transient Ca2+ increase. After restoration of the extracellular Ca2+ concentration to 2 mM, a dramatic Ca2+ increase occurred. This elevation was completely blocked by chloroquine and was markedly inhibited by Pyr3, a selective antagonist of transient receptor potential C3 (TRPC3) channel and stromal interaction molecule (STIM)/Orai channel. Furthermore, the TG-induced transient Ca2+ increase under Ca2+-free conditions was eliminated in the presence of chloroquine. Chloroquine also blocked the dialyzed inositol-1,4,5-trisphosphate (IP3)-induced intracellular Ca2+ increase. However, chloroquine was not able to decrease the caffeine-induced Ca2+ increase. Conclusion: These data indicate that chloroquine inhibits the elevation of intracellular Ca2+ in thymic CD4+ T cells by inhibiting IP3 receptor-mediated Ca2+ release from intracellular stores and TRPC3 channel-mediated and/or STIM/Orai channel-mediated Ca2+ influx.


2015 ◽  
Vol 22 (9) ◽  
pp. 992-1003 ◽  
Author(s):  
A. D. White ◽  
C. Sarfas ◽  
K. West ◽  
L. S. Sibley ◽  
A. S. Wareham ◽  
...  

ABSTRACTNine million cases of tuberculosis (TB) were reported in 2013, with a further 1.5 million deaths attributed to the disease. When delivered as an intradermal (i.d.) injection, theMycobacterium bovisBCG vaccine provides limited protection, whereas aerosol delivery has been shown to enhance efficacy in experimental models. In this study, we used the rhesus macaque model to characterize the mucosal and systemic immune response induced by aerosol-delivered BCG vaccine. Aerosol delivery of BCG induced both Th1 and Th17 cytokine responses. Polyfunctional CD4 T cells were detected in bronchoalveolar lavage (BAL) fluid and peripheral blood mononuclear cells (PBMCs) 8 weeks following vaccination in a dose-dependent manner. A similar trend was seen in peripheral gamma interferon (IFN-γ) spot-forming units measured by enzyme-linked immunosorbent spot (ELISpot) assay and serum anti-purified protein derivative (PPD) IgG levels. CD8 T cells predominantly expressed cytokines individually, with pronounced tumor necrosis factor alpha (TNF-α) production by BAL fluid cells. T-cell memory phenotype analysis revealed that CD4 and CD8 populations isolated from BAL fluid samples were polarized toward an effector memory phenotype, whereas the frequencies of peripheral central memory T cells increased significantly and remained elevated following aerosol vaccination. Expression patterns of the α4β1 integrin lung homing markers remained consistently high on CD4 and CD8 T cells isolated from BAL fluid and varied on peripheral T cells. This characterization of aerosol BCG vaccination highlights features of the resulting mycobacterium-specific immune response that may contribute to the enhanced protection previously reported in aerosol BCG vaccination studies and will inform future studies involving vaccines delivered to the mucosal surfaces of the lung.


2006 ◽  
Vol 119 ◽  
pp. S183
Author(s):  
Sheraz Yaqub ◽  
Tone Bryn ◽  
Milada Mahic ◽  
Einar Aandahl ◽  
Kjetil Tasken

2015 ◽  
Vol 195 (2) ◽  
pp. 564-575 ◽  
Author(s):  
Hana Moon ◽  
Chanho Park ◽  
Jae-Ghi Lee ◽  
Sang Hyuck Shin ◽  
Joo Hee Lee ◽  
...  

2016 ◽  
Vol 10 (2) ◽  
pp. 520-530 ◽  
Author(s):  
P A Romagnoli ◽  
H H Fu ◽  
Z Qiu ◽  
C Khairallah ◽  
Q M Pham ◽  
...  

2018 ◽  
Vol 9 ◽  
Author(s):  
Takashi Ogasawara ◽  
Yuko Kohashi ◽  
Jun Ikari ◽  
Toshibumi Taniguchi ◽  
Nobuhide Tsuruoka ◽  
...  

Rheumatology ◽  
2019 ◽  
Vol 58 (11) ◽  
pp. 2051-2060 ◽  
Author(s):  
Giovanni Almanzar ◽  
Felix Kienle ◽  
Marc Schmalzing ◽  
Anna Maas ◽  
Hans-Peter Tony ◽  
...  

AbstractObjectiveRA is a chronic inflammatory disease characterized by lymphocyte infiltration and release of inflammatory cytokines. Previous studies have shown that treatment with Janus kinase inhibitors, such as tofacitinib, increased the incidence rate of herpes zoster compared with conventional DMARDs. Therefore, this study aimed to investigate the effect of tofacitinib on the varicella-zoster-virus (VZV)-specific T cell immune response.MethodsThe effect of tofacitinib on the VZV-specific T cell immune response was determined by evaluating the IFNγ production, the proliferative capacity, the VZV-induced differentiation into effector and memory T cells, the expression of activation marker CD69 and helper T cell type 1 (Th1)-characteristic chemokine receptors, such as CXCR3 and CCR5, as well as cytotoxic activity (perforin and granzyme B expression) of CD4+ T cells of patients with RA compared with healthy donors upon stimulation with VZV antigen in vitro.ResultsTofacitinib significantly reduced the IFNγ production, proliferation, activation, and CXCR3 expression of VZV-specific CD4+ T cells in a dose-dependent manner in short- and long-term lymphocyte culture. No effect on the distribution of naive, effectors or memory, or on the expression of perforin or granzyme B by VZV-specific CD4+ T cells was observed.ConclusionThis study showed that tofacitinib significantly modulated the Th1 response to VZV. The poor VZV-specific cellular immune response in patients with RA may be considered in recommendations regarding appropriate vaccination strategies for enhancing the VZV-specific Th1 response.


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