scholarly journals Interleukin-15 Enhances Innate and Adaptive Immune Responses to Blood-Stage Malaria Infection in Mice

2005 ◽  
Vol 73 (5) ◽  
pp. 3172-3177 ◽  
Author(s):  
Rebecca Ing ◽  
Philippe Gros ◽  
Mary M. Stevenson

ABSTRACT Compared to C57BL/6 wild-type mice, interleukin-15−/− (IL-15−/−) mice showed delayed clearance of Plasmodium chabaudi AS infection, lower type 1 cytokine production, impaired dendritic cell and NK cell functions, and lower titers of malaria-specific antibodies. Thus, IL-15 supports early control and timely resolution of blood-stage malaria through promotion of Th1-dependent innate and adaptive immune responses.

2012 ◽  
Vol 12 (5) ◽  
pp. 705-716 ◽  
Author(s):  
Hong Zhao ◽  
Aki Konishi ◽  
Yukiko Fujita ◽  
Masanori Yagi ◽  
Keiichi Ohata ◽  
...  

Metabolism ◽  
2021 ◽  
pp. 154795
Author(s):  
Anna W.M. Janssen ◽  
Rinke Stienstra ◽  
Martin Jaeger ◽  
Alain J. van Gool ◽  
Leo A.B. Joosten ◽  
...  

2017 ◽  
Vol 8 (10) ◽  
pp. 3523-3532 ◽  
Author(s):  
Li-Xia He ◽  
Jin-Wei Ren ◽  
Rui Liu ◽  
Qi-He Chen ◽  
Jian Zhao ◽  
...  

Traditionally used as a restorative medicine, ginseng (Panax ginseng Meyer) has been widely used and acclaimed herb in Chinese communities for thousands of years.


2009 ◽  
Vol 206 (13) ◽  
pp. 3101-3114 ◽  
Author(s):  
Olga Schulz ◽  
Elin Jaensson ◽  
Emma K. Persson ◽  
Xiaosun Liu ◽  
Tim Worbs ◽  
...  

Chemokine receptor CX3CR1+ dendritic cells (DCs) have been suggested to sample intestinal antigens by extending transepithelial dendrites into the gut lumen. Other studies identified CD103+ DCs in the mucosa, which, through their ability to synthesize retinoic acid (RA), appear to be capable of generating typical signatures of intestinal adaptive immune responses. We report that CD103 and CX3CR1 phenotypically and functionally characterize distinct subsets of lamina propria cells. In contrast to CD103+ DC, CX3CR1+ cells represent a nonmigratory gut-resident population with slow turnover rates and poor responses to FLT-3L and granulocyte/macrophage colony-stimulating factor. Direct visualization of cells in lymph vessels and flow cytometry of mouse intestinal lymph revealed that CD103+ DCs, but not CX3CR1-expressing cells, migrate into the gut draining mesenteric lymph nodes (LNs) under steady-state and inflammatory conditions. Moreover, CX3CR1+ cells displayed poor T cell stimulatory capacity in vitro and in vivo after direct injection of cells into intestinal lymphatics and appeared to be less efficient at generating RA compared with CD103+ DC. These findings indicate that selectively CD103+ DCs serve classical DC functions and initiate adaptive immune responses in local LNs, whereas CX3CR1+ populations might modulate immune responses directly in the mucosa and serve as first line barrier against invading enteropathogens.


2009 ◽  
Vol 206 (10) ◽  
pp. 2235-2251 ◽  
Author(s):  
Seung-Hwan Lee ◽  
Kwang-Sin Kim ◽  
Nassima Fodil-Cornu ◽  
Silvia M. Vidal ◽  
Christine A. Biron

Natural killer (NK) cells have the potential to deliver both direct antimicrobial effects and regulate adaptive immune responses, but NK cell yields have been reported to vary greatly during different viral infections. Activating receptors, including the Ly49H molecule recognizing mouse cytomegalovirus (MCMV), can stimulate NK cell expansion. To define Ly49H's role in supporting NK cell proliferation and maintenance under conditions of uncontrolled viral infection, experiments were performed in Ly49h−/−, perforin 1 (Prf1)−/−, and wild-type (wt) B6 mice. NK cell numbers were similar in uninfected mice, but relative to responses in MCMV-infected wt mice, NK cell yields declined in the absence of Ly49h and increased in the absence of Prf1, with high rates of proliferation and Ly49H expression on nearly all cells. The expansion was abolished in mice deficient for both Ly49h and Prf1 (Ly49h−/−Prf1−/−), and negative consequences for survival were revealed. The Ly49H-dependent protection mechanism delivered in the absence of Prf1 was a result of interleukin 10 production, by the sustained NK cells, to regulate the magnitude of CD8 T cell responses. Thus, the studies demonstrate a previously unappreciated critical role for activating receptors in keeping NK cells present during viral infection to regulate adaptive immune responses.


2010 ◽  
Vol 184 (5) ◽  
pp. 2377-2385 ◽  
Author(s):  
Aniko Csillag ◽  
Istvan Boldogh ◽  
Kitti Pazmandi ◽  
Zoltan Magyarics ◽  
Peter Gogolak ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-18 ◽  
Author(s):  
Margarida Lima ◽  
Magdalena Leander ◽  
Marlene Santos ◽  
Ana Helena Santos ◽  
Catarina Lau ◽  
...  

Studies of chemokine receptors (CKR) in natural killer- (NK-) cells have already been published, but only a few gave detailed information on its differential expression on blood NK-cell subsets. We report on the expression of the inflammatory and homeostatic CKR on normal bloodCD56+lowCD16+andCD56+high  CD16-/+lowNK-cells. ConventionalCD56+lowandCD56+highNK-cells present in the normal PB do express CKR for inflammatory cytokines, although with different patternsCD56+lowNK-cells are mainly CXCR1/CXCR2+and CXCR3/CCR5−/+, whereas mostlyCD56+highNK-cells are CXCR1/CXCR2−and CXCR3/CCR5+. Both NK-cell subsets have variable CXCR4 expression and are CCR4−and CCR6−. The CKR repertoire of theCD56+lowNK-cells approaches to that of neutrophils, whereas the CKR repertoire of theCD56+highNK-cells mimics that of Th1+T cells, suggesting that these cells are prepared to migrate into inflamed tissues at different phases of the immune response. In addition, we describe a subpopulation of NK-cells with intermediate levels of CD56 expression, which we namedCD56+intNK-cells. These NK-cells are CXCR3/CCR5+, they have intermediate levels of expression of CD16, CD62L, CD94, and CD122, and they are CD57−and CD158a−. In view of their phenotypic features, we hypothesize that they correspond to a transitional stage, between the well-knownCD56+highandCD56+lowNK-cells populations.


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