scholarly journals Sulfatide-activated type II NKT cells suppress immunogenic maturation of lung dendritic cells in murine models of asthma

2019 ◽  
Vol 317 (5) ◽  
pp. L578-L590
Author(s):  
Huaqin Pan ◽  
Guqin Zhang ◽  
Hanxiang Nie ◽  
Shuhua Li ◽  
Shaojun He ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Airway Inflammation ◽  
Mouse Models ◽  
Adoptive Transfer ◽  
Allergic Airway Inflammation ◽  
Nkt Cells ◽  
Type I ◽  
Type Ii ◽  
Functional Maturation

Our previous study showed that sulfatide-activated type II natural killer T (NKT) cells can prevent allergic airway inflammation in an ovalbumin (OVA)-induced murine model of asthma, but the underlying mechanism is unclear. Recently, sulfatide-activated type II NKT cells were shown to modulate the function of dendritic cells in experimental autoimmune encephalomyelitis and nonobese diabetic mice. Thus, it was hypothesized that sulfatide-activated type II NKT cells may modulate the function of lung dendritic cells (LDCs) in asthmatic mice. Our data showed that, in our mouse models, activation of type II NKT cells by sulfatide administration and adoptive transfer of sulfatide-activated type II NKT cells resulted in reduced expression of surface maturation markers and proinflammatory cytokine production of LDCs. LDCs from sulfatide-treated asthmatic mice, in contrast to LDCs from PBS-treated asthmatic mice, significantly reduced allergic airway inflammation in vivo. However, we found no influence of sulfatide-activated type II NKT cells on the phenotypic and functional maturation of bone marrow-derived dendritic cells in vitro. In addition, adoptive transfer of sulfatide-activated type II NKT cells did not influence the phenotypic and functional maturation of LDCs in CD1d−/− mice, which lack both type I and II NKT cells, immunized and challenged with OVA. Our data reveal that sulfatide-activated type II NKT cells can suppress immunogenic maturation of LDCs to reduce allergic airway inflammation in mouse models of asthma, and it is possible that the immunomodulatory effect needs type I NKT cells.

Sulfatide-activated type II NKT cells prevent allergic airway inflammation by inhibiting type I NKT cell function in a mouse model of asthma

2011 ◽  
Vol 301 (6) ◽  
pp. L975-L984 ◽  
Author(s):  
Guqin Zhang ◽  
Hanxiang Nie ◽  
Jiong Yang ◽  
Xuhong Ding ◽  
Yi Huang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Cell Activation ◽  
Cell Function ◽  
Allergic Airway Inflammation ◽  
Nkt Cells ◽  
Chronic Inflammatory Disease ◽  
Type I ◽  
Type Ii ◽  
Nkt Cell

Asthma is a common chronic inflammatory disease involving many different cell types. Recently, type I natural killer T (NKT) cells have been demonstrated to play a crucial role in the development of asthma. However, the roles of type II NKT cells in asthma have not been investigated before. Interestingly, type I and type II NKT cells have been shown to have opposing roles in antitumor immunity, antiparasite immunity, and autoimmunity. We hypothesized that sulfatide-activated type II NKT cells could prevent allergic airway inflammation by inhibiting type I NKT cell function in asthma. Strikingly, in our mouse model, activation of type II NKT cells by sulfatide administration and adoptive transfer of sulfatide-activated type II NKT cells result in reduced-inflammation cell infiltration in the lung and bronchoalveolar lavage fluid, decreased levels of IL-4 and IL-5 in the BALF; and decreased serum levels of ovalbumin-specific IgE and IgG1. Furthermore, it is found that the activation of sulfatide-reactive type II NKT cells leads to the functional inactivation of type I NKT cells, including the proliferation and cytokine secretion. Our data reveal that type II NKT cells activated by glycolipids, such as sulfatide, may serve as a novel approach to treat allergic diseases and other disorders characterized by inappropriate type I NKT cell activation.

scholarly journals The Toxoplasma gondii-Shuttling Function of Dendritic Cells Is Linked to the Parasite Genotype

2009 ◽  
Vol 77 (4) ◽  
pp. 1679-1688 ◽  
Author(s):  
Henrik Lambert ◽  
Polya P. Vutova ◽  
William C. Adams ◽  
Karin Loré ◽  
Antonio Barragan
Keyword(s):  
Dendritic Cells ◽  
Toxoplasma Gondii ◽  
Phenotypic Traits ◽  
Type I ◽  
Type Ii ◽  
Parasite Genotype ◽  
Type Iii ◽  
Parasite Motility

ABSTRACT Following intestinal invasion, the processes leading to systemic dissemination of the obligate intracellular protozoan Toxoplasma gondii remain poorly understood. Recently, tachyzoites representative of type I, II and III T. gondii populations were shown to differ with respect to their ability to transmigrate across cellular barriers. In this process of active parasite motility, type I strains exhibit a migratory capacity superior to those of the type II and type III strains. Data also suggest that tachyzoites rely on migrating dendritic cells (DC) as shuttling leukocytes to disseminate in tissue, e.g., the brain, where cysts develop. In this study, T. gondii tachyzoites sampled from the three populations were allowed to infect primary human blood DC, murine intestinal DC, or in vitro-derived DC and were compared for different phenotypic traits. All three archetypical lineages of T. gondii induced a hypermigratory phenotype in DC shortly after infection in vitro. Type II (and III) strains induced higher migratory frequency and intensity in DC than type I strains did. Additionally, adoptive transfer of infected DC favored the dissemination of type II and type III parasites over that of type I parasites in syngeneic mice. Type II parasites exhibited stronger intracellular association with both CD11c+ DC and other leukocytes in vivo than did type I parasites. Altogether, these findings suggest that infected DC contribute to parasite propagation in a strain type-specific manner and that the parasite genotype (type II) most frequently associated with toxoplasmosis in humans efficiently exploits DC migration for parasite dissemination.

scholarly journals The Role of NKT Cells in Glioblastoma

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1641
Author(s):  
Emily E. S. Brettschneider ◽  
Masaki Terabe
Keyword(s):  
Immune Responses ◽  
Cell Activity ◽  
Nkt Cells ◽  
Type I ◽  
Type Ii ◽  
Central Nervous System Diseases ◽  
Nkt Cell ◽  
Lipid Antigens ◽  
Immunoregulatory Mechanisms

Glioblastoma is an aggressive and deadly cancer, but to date, immunotherapies have failed to make significant strides in improving prognoses for glioblastoma patients. One of the current challenges to developing immunological interventions for glioblastoma is our incomplete understanding of the numerous immunoregulatory mechanisms at play in the glioblastoma tumor microenvironment. We propose that Natural Killer T (NKT) cells, which are unconventional T lymphocytes that recognize lipid antigens presented by CD1d molecules, may play a key immunoregulatory role in glioblastoma. For example, evidence suggests that the activation of type I NKT cells can facilitate anti-glioblastoma immune responses. On the other hand, type II NKT cells are known to play an immunosuppressive role in other cancers, as well as to cross-regulate type I NKT cell activity, although their specific role in glioblastoma remains largely unclear. This review provides a summary of our current understanding of NKT cells in the immunoregulation of glioblastoma as well as highlights the involvement of NKT cells in other cancers and central nervous system diseases.

Modeling Endoleaks and Collateral Reperfusion following Endovascular AAA Exclusion

2003 ◽  
Vol 10 (3) ◽  
pp. 424-432 ◽  
Author(s):  
Chuh K. Chong ◽  
Thien V. How ◽  
Geoffrey L. Gilling-Smith ◽  
Peter L. Harris
Keyword(s):  
Stent Graft ◽  
Aortic Pressure ◽  
Type I ◽  
Type Ii ◽  
Pump System ◽  
Type Ii Endoleak ◽  
Type I Endoleak ◽  
The Impact ◽  
Mean Aortic Pressure

Purpose: To investigate the effect on intrasac pressure of stent-graft deployment within a life-size silicone rubber model of an abdominal aortic aneurysm (AAA) maintained under physiological conditions of pressure and flow. Methods: A commercial bifurcated device with the polyester fabric preclotted with gelatin was deployed in the AAA model. A pump system generated physiological flow. Mean and pulse aortic and intrasac pressures were measured simultaneously using pressure transducers. To simulate a type I endoleak, plastic tubing was placed between the aortic wall and the stent-graft at the proximal anchoring site. Type II endoleak was simulated by means of side branches with set inflow and outflow pressures and perfusion rates. Type IV endoleak was replicated by removal of gelatin from the graft fabric. Results: With no endoleak, the coated graft reduced the mean and pulse sac pressures to negligible values. When a type I endoleak was present, mean sac pressure reached a value similar to mean aortic pressure. When net flow through the sac due to a type II endoleak was present, mean sac pressure was a function of the inlet pressure, while pulse pressure in the sac was dependent on both inlet and outlet pressures. As perfusion rates increased, both mean and pulse sac pressures decreased. When there was no outflow, mean sac pressure was similar to mean aortic pressure. In the presence of both type I and type II endoleaks, mean sac pressure reached mean aortic pressure when the net perfusion rate was low. Conclusions: In vitro studies are useful in gaining an understanding of the impact of different types of endoleaks, in isolation and in combination, on intrasac pressure after aortic stent-graft deployment.

Amelioration of allergic airway inflammation in mice by regulatory IL-35 through dampening inflammatory dendritic cells

Allergy ◽  
2015 ◽  
Vol 70 (8) ◽  
pp. 921-932 ◽  
Author(s):  
J. Dong ◽  
C. K. Wong ◽  
Z. Cai ◽  
D. Jiao ◽  
M. Chu ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Inflammatory Dendritic Cells

Type VI collagen expression is upregulated in the early events of chondrocyte differentiation

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 245-251
Author(s):  
R. Quarto ◽  
B. Dozin ◽  
P. Bonaldo ◽  
R. Cancedda ◽  
A. Colombatti
Keyword(s):  
Suspension Culture ◽  
Type I Collagen ◽  
Type Ii Collagen ◽  
Type I ◽  
Type Ii ◽  
Type Vi Collagen ◽  
Full Spectrum ◽  
Collagen Expression ◽  
Hypertrophic Chondrocyte

Dedifferentiated chondrocytes cultured adherent to the substratum proliferate and synthesize large amounts of type I collagen but when transferred to suspension culture they decrease proliferation, resume the chondrogenic phenotype and the synthesis of type II collagen, and continue their maturation to hypertrophic chondrocyte (Castagnola et al., 1986, J. Cell Biol. 102, 2310–2317). In this report, we describe the developmentally regulated expression of type VI collagen in vitro in differentiating avian chondrocytes. Type VI collagen mRNA is barely detectable in dedifferentiated chondrocytes as long as the attachment to the substratum is maintained, but increases very rapidly upon passage of the cells into suspension culture reaching a peak after 48 hours and declining after 5–6 days of suspension culture. The first evidence of a rise in the mRNA steady-state levels is obtained already at 6 hours for the alpha 3(VI) chain. Immunoprecipitation of metabolically labeled cells with type VI collagen antibodies reveals that the early mRNA rise is paralleled by an increased secretion of type VI collagen in cell media. Induction of type VI collagen is not the consequence of trypsin treatment of dedifferentiated cells since exposure to the actin-disrupting drug cytochalasin or detachment of the cells by mechanical procedures has similar effects. In 13-day-old chicken embryo tibiae, where the full spectrum of the chondrogenic differentiation process is represented, expression of type VI collagen is restricted to the articular cartilage where chondrocytes developmental stage is comparable to stage I (high levels of type II collagen expression).(ABSTRACT TRUNCATED AT 250 WORDS)

Congenital Dyserythropoietic Anemia

PEDIATRICS ◽  
1973 ◽  
Vol 51 (5) ◽  
pp. 957-958
Author(s):  
G. Bennett Humphrey ◽  
Bahaod-Din Mojab ◽  
Ingomar Mutz
Keyword(s):  
Carbohydrate Metabolism ◽  
Morphological Characteristics ◽  
Type I ◽  
Type Ii ◽  
Congenital Dyserythropoietic Anemia ◽  
The 1950S ◽  
Deja Vu ◽  
Déjà Vu ◽  
Excellent Article

Reading the excellent article by Drs. Murphy and Oski, "Congenital Dyserythropoietic Anemia (CDA)",1 which further defines type II, produced a sense of deja vu. In the 1950s, nonspherocytic, hemolytic anemias (HNHA) were categorized as type I and II based on the in vitro autohemolysis test.2 This group of anemias has subsequently been demonstrated to be due to a series of enzymatic abnormalities in carbohydrate metabolism.3 In CDA, the morphological characteristics which define types I, II, and III probably reflect nuclear rather than cytoplasmic abnormalities.

Sign in / Sign up

Export Citation Format

Share Document