Plasmacytoid dendritic cells and myeloid cells differently contribute to BAFF over-expression during primary HIV infection

AIDS ◽  
2015 ◽  
pp. 1 ◽  
Author(s):  
Gwenoline Borhis ◽  
Chantal Burelout ◽  
Nada Chaoul ◽  
Nikaïa Smith ◽  
Cecile Goujard ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Hiv Infection ◽  
Myeloid Cells ◽  
Plasmacytoid Dendritic Cells ◽  
Primary Hiv Infection ◽  
Over Expression

PLASMACYTOID DENDRITIC CELLS FUNCTION IN HIV INFECTION

2008 ◽  
Vol 31 (4) ◽  
pp. 13
Author(s):  
Martin Hyrcza ◽  
Mario Ostrowski ◽  
Sandy Der
Keyword(s):  
Dendritic Cells ◽  
Influenza Virus ◽  
Hiv Infection ◽  
Gene Transcription ◽  
Sendai Virus ◽  
Plasmacytoid Dendritic Cells ◽  
Type I Interferons ◽  
Interferon Response ◽  
Type I ◽  
Type I Ifn

Plasmacytoid dendritic cells (pDCs) are innate immune cells able to produce large quantities of type I interferons (IFN) when activated. Human immunodeficiency virus (HIV)-infected patients show generalized immune dysfunction characterized in part by chronic interferon response. In this study we investigated the role of dendritic cells inactivating and maintaining this response. Specifically we compared the IFN geneactivity in pDCs in response to several viruses and TLR agonists. We hypothesized that 1) the pattern of IFN gene transcription would differ in pDCs treated with HIV than with other agents, and 2) that pDCs from patients from different stages of disease would respond differently to the stimulations. To test these hypotheses, we obtained pDCs from 15 HIV-infected and uninfected individuals and treated freshly isolated pDCs with either HIV (BAL strain), influenza virus (A/PR/8/34), Sendai virus (Cantell strain), TLR7 agonist(imiquimod), or TLR9 agonist (CpG-ODN) for 6h. Type I IFN gene transcription was monitored by real time qPCRfor IFNA1, A2, A5, A6, A8,A17, B1, and E1, and cytokine levels were assayed by Cytometric Bead Arrays forTNF?, IL6, IL8, IL10, IL1?, and IL12p70. pDC function as determined by these two assays showed no difference between HIV-infected and uninfected patients or between patients with early or chronic infection. Specifically, HIV did notinduce type I IFN gene expression, whereas influenza virus, Sendai virus and imiquimod did. Similarly, HIV failed to induce any cytokine release from pDCs in contrast to influenza virus, Sendai virus and imiquimod, which stimulatedrelease of TNF?, IL6, or IL8. Together these results suggest that the reaction of pDCs to HIV virus is quantitatively different from the response to agents such as virus, Sendai virus, and imiquimod. In addition, pDCs from HIV-infected persons have responses similar to pDCs from uninfected donors, suggesting, that the DC function may not be affected by HIV infection.

Abstract 107: Depletion of Plasmacytoid Dendritic Cells Inhibits Experimental Abdominal Aortic Aneurysms

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Baohui Xu ◽  
Haojun Xuan ◽  
Naoki Fujimura ◽  
Sara A Michie ◽  
Ronald L Dalman
Keyword(s):  
Dendritic Cells ◽  
Inflammatory Diseases ◽  
Myeloid Cells ◽  
Abdominal Aortic Aneurysms ◽  
Plasmacytoid Dendritic Cells ◽  
Aortic Aneurysms ◽  
Major Type ◽  
Abdominal Aortic

Introduction: Abdominal aortic aneurysms (AAA) manifest histologic features consistent with other chronic inflammatory diseases. Infiltrating mural myeloid cells (e.g. macrophages) are already recognized as important contributors to aneurysm pathogenesis, however, the role of plasmacytoid dendritic cells (pDC), major type 1 interferon-producing myeloid cells involving in autoimmune diseases and atherosclerosis, has not been previously investigated in this context. Methods and Results: AAAs were created in 12 week old male C57BL/6J mice by transient intra-aortic infusion of porcine pancreatic elastase (PPE). AAA development and progression were assessed via serial ultrasound determination of aortic diameter in vivo , and histology at sacrifice. The fraction of circulating leukocytes identified as pDCs was significantly increased immediately following PPE infusion (aneurysm initiation). Treatment with mPDCA-1 mAb (400 μg i.p. q.o.d.), beginning one day prior to PPE infusion, depleted more than 90% of bone marrow, spleen and peripheral blood pDCs (data not shown) and suppressed subsequent aneurysm development and progression compared to that noted in PPE-infused mice treated with control mAb. mPDCA-1 treatment promoted aortic medial elastin and smooth muscle preservation, while limiting mural macrophage accumulation and neocapillary formation. Conclusion: These findings suggest a role for plasmacytoid dendritic cells in promoting the initiation and progression of experimental abdominal aortic aneurysms.

scholarly journals Plasmacytoid dendritic cells in HIV infection: striking a delicate balance

2010 ◽  
Vol 87 (4) ◽  
pp. 609-620 ◽  
Author(s):  
Patricia Fitzgerald-Bocarsly ◽  
Evan S. Jacobs
Keyword(s):  
Dendritic Cells ◽  
Hiv Infection ◽  
Plasmacytoid Dendritic Cells ◽  
Delicate Balance

Deregulation of the expression of the fractalkine/fractalkine receptor complex in HIV-1–infected patients

Blood ◽  
2001 ◽  
Vol 98 (6) ◽  
pp. 1678-1686 ◽  
Author(s):  
Arnaud Foussat ◽  
Laurence Bouchet-Delbos ◽  
Dominique Berrebi ◽  
Ingrid Durand-Gasselin ◽  
Aurore Coulomb-L'Hermine ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Cell ◽  
Hiv Infection ◽  
Plasma Cells ◽  
Receptor Gene ◽  
Plasmacytoid Dendritic Cells ◽  
Antiretroviral Drugs ◽  
Receptor Complex ◽  
Fractalkine Receptor ◽  
And Migration

Abstract Fractalkine is the only member of the CX3C chemokine family. Polymorphism of the fractalkine receptor gene may influence the prognosis of human immunodeficiency virus (HIV) infection, but the nature of the cells expressing fractalkine or its receptor in HIV-infected patients remains unknown. We show that, in contrast to HIV-uninfected individuals, a large number of cells expressed fractalkine in T-cell zones of lymph nodes from HIV-infected patients. CD83+ mature and CD123+ plasmacytoid dendritic cells as well as plasma cells are involved in this increased expression of fractalkine. Increased numbers of plasmacytoid dendritic cells and plasma cells were present in T-cell zones of HIV-infected patients. CD83+ dendritic cells were present in similar number in HIV-infected patients and controls, but an increased fraction of these cells produced fractalkine in HIV-infected patients. Many plasma cells in the gut-associated lymphoid tissue from HIV-infected patients also produced fractalkine, whereas few cells produced fractalkine in the gut of controls. The fraction of CD45RO+ and CD45RO− T helper (Th) cells expressing the fractalkine receptor CX3CR1 was higher in HIV-infected patients than in healthy individuals, and these cells were abnormally sensitive to fractalkine stimulation. This increased response correlated with HIV viremia, and it returned to normal levels in patients successfully treated with antiretroviral drugs. The increased expression of the fractalkine/fractalkine receptor complex associated with HIV infection may affect adhesion and migration of Th lymphocytes and their interaction with dendritic cells. Thus, it may influence the equilibrium between depletion and renewal of the Th lymphocyte compartment.

scholarly journals M27 Expressed by Cytomegalovirus Counteracts Effective Type I Interferon Induction of Myeloid Cells but Not of Plasmacytoid Dendritic Cells

2014 ◽  
Vol 88 (23) ◽  
pp. 13638-13650 ◽  
Author(s):  
M. Doring ◽  
I. Lessin ◽  
T. Frenz ◽  
J. Spanier ◽  
A. Kessler ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Type I Interferon ◽  
Myeloid Cells ◽  
Plasmacytoid Dendritic Cells ◽  
Type I ◽  
Interferon Induction

scholarly journals Flt3L-Mediated Expansion of Plasmacytoid Dendritic Cells Suppresses HIV Infection in Humanized Mice

Cell Reports ◽  
2019 ◽  
Vol 29 (9) ◽  
pp. 2770-2782.e5 ◽  
Author(s):  
Tram N.Q. Pham ◽  
Oussama Meziane ◽  
Mohammad Alam Miah ◽  
Olga Volodina ◽  
Chloé Colas ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Hiv Infection ◽  
Plasmacytoid Dendritic Cells ◽  
Humanized Mice

scholarly journals Sex Differences in Primary HIV Infection: Revisiting the Role of TLR7-Driven Type 1 IFN Production by Plasmacytoid Dendritic Cells in Women

2021 ◽  
Vol 12 ◽  
Author(s):  
Jean-Charles Guéry
Keyword(s):  
Dendritic Cells ◽  
Hiv Infection ◽  
X Chromosome ◽  
Type I Interferon ◽  
Acute Infection ◽  
Plasmacytoid Dendritic Cells ◽  
Type I ◽  
Hiv 1 ◽  
Tlr7 Stimulation

Plasmacytoid dendritic cells (pDCs) produce type I interferon (IFN-I) during HIV-1 infection in response to TLR7 stimulation. However, IFN-I-signaling has been shown to play opposite effects in HIV-1 and SIV infection. TLR7-driven type I interferon production in pDCs is higher in women than in men due to the cell-intrinsic actions of estrogen and X-chromosome complement. Indeed, TLR7 is encoded on the X-chromosome, and the TLR7 gene escapes the X-chromosome inactivation in immune cells of women which express significantly higher levels of TLR7 protein than male cells. Following HIV infection, women have a lower viremia during acute infection and exhibit stronger antiviral responses than men, which has been attributed to the increased capacity of female pDCs to produce IFN-α upon TLR7-stimulation. However, a deleterious functional impact of an excessive TLR7 response on acute viremia in women has been recently revealed by the analysis of the frequent rs179008 c.32A>T SNP of TLR7. This SNP was identified as a sex-specific protein abundance quantitative trait locus (pQTL) causing a difference in the TLR7 protein dosage and effector function in females only. T allele expression was associated with a lower TLR7 protein synthesis, blunted production of IFN-α by pDCs upon TLR7 stimulation, and an unexpectedly lower viral load during primary HIV-1 infection in women. In the present review, the author will revisit the role of TLR7-driven pDC innate function in the context of HIV-1 infection to discuss at what stage of primary HIV-1 infection the TLR7 rs179008 T allele is likely to be protective in women.

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