scholarly journals Host Transcriptional Response to Persistent Infection with a Live-Attenuated Porcine Reproductive and Respiratory Syndrome Virus Strain

Viruses ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 817
Author(s):  
Jayeshbhai Chaudhari ◽  
Chia-Sin Liew ◽  
Aspen M. Workman ◽  
Jean-Jack M. Riethoven ◽  
David Steffen ◽  
...  
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Lymphoid Tissue ◽  
Innate Immune ◽  
Respiratory Syndrome Virus ◽  
Lymphoid Tissues ◽  
Innate Immune Responses ◽  
Cell Homing ◽  
T Cell Homing ◽  
Prrsv Strain

Both virulent and live-attenuated porcine reproductive and respiratory syndrome virus (PRRSV) strains can establish persistent infection in lymphoid tissues of pigs. To investigate the mechanisms of PRRSV persistence, we performed a transcriptional analysis of inguinal lymphoid tissue collected from pigs experimentally infected with an attenuated PRRSV strain at 46 days post infection. A total of 6404 differentially expressed genes (DEGs) were detected of which 3960 DEGs were upregulated and 2444 DEGs were downregulated. Specifically, genes involved in innate immune responses and chemokines and receptors associated with T-cell homing to lymphoid tissues were down regulated. As a result, homing of virus-specific T-cells to lymphoid tissues seems to be ineffective, evidenced by the lower frequencies of virus-specific T-cell in lymphoid tissue than in peripheral blood. Genes associated with T-cell exhaustion were upregulated. Likewise, genes involved in the anti-apoptotic pathway were upregulated. Collectively, the data suggested that the live-attenuated PRRSV strain establishes a pro-survival microenvironment in lymphoid tissue by suppressing innate immune responses, T-cell homing, and preventing cell apoptosis.

scholarly journals Decoding the role of CBLB for innate immune responses regulating systemic dissemination during Non-Tuberculous Mycobacteria infection

2020 ◽  
Author(s):  
Srinivasu Mudalagiriyappa ◽  
Jaishree Sharma ◽  
Hazem F. M. Abdelaal ◽  
Thomas C. Kelly ◽  
Woosuk Choi ◽  
...  
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Granulomatous Inflammation ◽  
Innate Immune ◽  
Dependent Manner ◽  
Innate Immune Responses ◽  
Inflammatory Monocytes ◽  
Cell Immunity

AbstractNon-Tuberculous Mycobacteria (NTM) are ubiquitous in nature, present in soil and water, and cause primary leading to disseminated infections in immunocompromised individuals. NTM infections are surging in recent years due to an increase in an immune-suppressed population, medical interventions, and patients with underlying lung diseases. Host regulators of innate immune responses, frontiers for controlling infections and dissemination, are poorly defined during NTM infections. Here, we describe the role of CBLB, an E3-ubiquitin ligase, for innate immune responses and disease progression in a mouse model of NTM infection under compromised T-cell immunity. We found that CBLB thwarted NTM growth and dissemination in a time- and infection route- dependent manner. Mechanistically, we uncovered defects in many innate immune cells in the absence of Cblb, including poor responses of NK cells, inflammatory monocytes, and conventional dendritic cells. Strikingly, Cblb-deficient macrophages were competent to control NTM growth in vitro. Histopathology suggested the lack of early formation of granulomatous inflammation in the absence of CBLB. Collectively, CBLB is essential to mount productive innate immune responses and help prevent the dissemination during an NTM infection under T-cell deficiency.

Impact of Immunosuppressive Drugs on Adaptive and Innate Immune Responses to Aspergillus fumigatus Antigens.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2222-2222
Author(s):  
Holger Hebart ◽  
Andreas Mickan ◽  
Ziad Haddad ◽  
Juergen Loeffler ◽  
Jean-Paul Latge ◽  
...  
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Invasive Aspergillosis ◽  
Immunosuppressive Agents ◽  
T Cell Responses ◽  
Innate Immune ◽  
Strong Impact ◽  
Innate Immune Responses ◽  
Cell Responses ◽  
The Impact

Abstract Appropriate activation of the innate and adaptive immune system is crucial for the successful control of invasive aspergillosis (IA). Acute and chronic graft-versus-host disease as well as corticosteroids were described as major risk factors for the development of IA. In this study, we assessed the impact of immunosuppressive agents (dexamethasone, rapamycin, Cyclosporin A, FK506) on the A. fumigatus induced activation of monocyte-derived immature dendritic cells (iDC) and A. fumigatus-specific T-cell responses in well established cell culture models. Immature DCs were found to be activated and to differentiate into mature DCs in response to A. fumigatus antigens. The upregulation of CD86 was inhibited by dexamethasone (D) in 3 out of 3 experiments, and of CD40 and CD80 in 2/3. CSA and FK506 had a variable impact on the upregulation of CD86, but not on CD40 and CD80, whereas the expression of co-stimulatory molecules was found unchanged upon incubation with rapamycin. Autologous DCs were found to restore A. fumigatus-specific T-cell responses. T-cell proliferation to A. fumigatus hyphae and a cellular extract of the culture filtrate were found to be strongly inhibited by rapamycin and dexamethasone (n=3), whereas the effect of CSA and FK506 (n=3) at the concentrations analysed was variable. The release of IFN-g in culture supernatants upon stimulation with A. fumigatus antigens was strongly reduced in the presence of rapamycin (n=3), whereas the release of IL-4 was found to be increased in the majority of experiments (n=3). Comparable results were observed upon stimulation with tetanus toxoid and a CMV lysate (n=3). These data indicate, that A. fumigatus-spec. T-cell responses may be directed towards a TH2 phenotype in the presence of immunosuppressive agents. In summary, immunosuppressive agents were found to exert differential effects on adaptive and innate immune responses directed against A. fumigatus. Whereas dexamethasone was found to modulate the expression of co-stimulatory molecules on A. fumigatus activated iDCs and to suppress A. fumigatus-specific lymphoproliferation, rapamycin exerted only minor effects on DC-activation but had a strong impact on A. fumigatus-induced T-cell responses. These results may help to tailor immunosuppressive regimens in patients at high risk for invasive aspergillosis.

Innate Immune Responses to Replication of Porcine Reproductive And Respiratory Syndrome Virus in Isolated Swine Alveolar Macrophages

2007 ◽  
Vol 20 (1) ◽  
pp. 105-118 ◽  
Author(s):  
Tahar Ait-Ali ◽  
Alison D. Wilson ◽  
David G. Westcott ◽  
Mary Clapperton ◽  
Martin Waterfall ◽  
...  
Keyword(s):  
Immune Responses ◽  
Alveolar Macrophages ◽  
Innate Immune ◽  
Respiratory Syndrome Virus ◽  
Innate Immune Responses

scholarly journals IL-17A in Human Respiratory Diseases: Innate or Adaptive Immunity? Clinical Implications

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Dominique M. A. Bullens ◽  
Ann Decraene ◽  
Sven Seys ◽  
Lieven J. Dupont
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Respiratory Diseases ◽  
Inflammatory Diseases ◽  
Cell Lineage ◽  
Innate Immune ◽  
Clinical Implications ◽  
Innate Immune Cells ◽  
Innate Immune Responses

Since the discovery of IL-17 in 1995 as a T-cell cytokine, inducing IL-6 and IL-8 production by fibroblasts, and the report of a separate T-cell lineage producing IL-17(A), called Th17 cells, in 2005, the role of IL-17 has been studied in several inflammatory diseases. By inducing IL-8 production and subsequent neutrophil attraction towards the site of inflammation, IL-17A can link adaptive and innate immune responses. More specifically, its role in respiratory diseases has intensively been investigated. We here review its role in human respiratory diseases and try to unravel the question whether IL-17A only provides a link between the adaptive and innate respiratory immunity or whether this cytokine might also be locally produced by innate immune cells. We furthermore briefly discuss the possibility to reduce local IL-17A production as a treatment option for respiratory diseases.

Disparate lymphoid chemokine expression in mice and men: no evidence of CCL21 synthesis by human high endothelial venules

Blood ◽  
2005 ◽  
Vol 106 (2) ◽  
pp. 444-446 ◽  
Author(s):  
Hege S. Carlsen ◽  
Guttorm Haraldsen ◽  
Per Brandtzaeg ◽  
Espen S. Baekkevold
Keyword(s):  
T Cell ◽  
Lymphoid Tissues ◽  
Human Tissues ◽  
High Endothelial Venules ◽  
Chemokine Production ◽  
Cell Homing ◽  
Cell Recruitment ◽  
T Cell Homing ◽  
Cc Chemokine Receptor 7 ◽  
Naive T Lymphocytes

Abstract T-cell homing to secondary lymphoid tissues generally depends on chemokine-induced firm adhesion in high endothelial venules (HEVs) and is primarily mediated through the CC chemokine receptor 7 (CCR7) on lymphocytes. The CCR7 ligand designated CCL21 is considered the most important trigger because it appears constitutively expressed by murine HEVs. Surprisingly, when we analyzed human tissues, no CCL21 mRNA could be detected in HEVs. In fact, CCL21 mRNA was only expressed in extravascular T-zone cells and lymphatics, whereas immunostaining revealed CCL21 protein within HEVs. This suggests that T-cell recruitment to human lymphoid tissues depends on the transcytosis of lymphoid chemokines through HEV cells because there is at present no evidence of alternative chemokine production in these cells that could explain the attraction of naive T lymphocytes.

Modulation of innate immune responses during human T-cell leukemia virus (HTLV-1) pathogenesis

2011 ◽  
Vol 22 (4) ◽  
pp. 197-210 ◽  
Author(s):  
Stéphanie Olière ◽  
Renée Douville ◽  
Alexandre Sze ◽  
S. Mehdi Belgnaoui ◽  
John Hiscott
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Leukemia Virus ◽  
Innate Immune ◽  
T Cell Leukemia ◽  
Innate Immune Responses ◽  
Cell Leukemia ◽  
Human T Cell ◽  
T Cell Leukemia Virus
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