Cellular immune response in Rhodnius prolixus: Role of ecdysone in hemocyte phagocytosis

2006 ◽  
Vol 52 (7) ◽  
pp. 711-716 ◽  
Author(s):  
Marcela B. Figueiredo ◽  
Daniele P. Castro ◽  
Nadir F. S. Nogueira ◽  
Eloi S. Garcia ◽  
Patrícia Azambuja
2019 ◽  
Vol 20 (2) ◽  
pp. 271 ◽  
Author(s):  
Przemyslaw Zdziarski

Although the existing paradigm states that cytomegalovirus (CMV) reactivation is under the control of the cellular immune response, the role of humoral and innate counterparts are underestimated. The study analyzed the host–virus interaction i.e., CMV-immune response evolution during infection in three different clinical situations: (1) immunodeficient CMV-positive human leukocyte antigen (HLA)-matched bone marrow recipients after immunoablative conditioning as well as immunocompetent, (2) adult, and (3) infant with primary immune response. In the first situation, a fast and significant decrease of specific immunity was observed but reconstitution of marrow-derived B and natural killer (NK) cells was observed prior to thymic origin of T cells. The lowest CMV-IgG (93.2 RU/mL) was found just before CMV viremia. It is noteworthy that the sole and exclusive factor of CMV-specific immune response is a residual recipient antibody class IgG. The CMV-quantiferon increase was detected later, but in the first phase, phytohemagglutinin (PHA)-induced IFN-γ release was significantly lower than that of CMV-induced (“indeterminate” results). It corresponds with the increase of NK cells at the top of lymphocyte reconstitution and undetected CMV-specific CD8 cells using a pentamer technique. In immunocompetent adult (CMV-negative donor), the cellular and humoral immune response increased in a parallel manner, but symptoms of CMV mononucleosis persisted until the increase of specific IgG. During infancy, the decrease of the maternal CMV-IgG level to 89.08 RU/mL followed by clinical sequel, i.e., CMV replication, were described. My observations shed light on a unique host-CMV interaction and CMV-IgG role: they indicate that its significant decrease predicts CMV replication. Before primary cellular immune response development, the high level of residual CMV-IgG (about >100 R/mL) from mother or recipient prevents virus reactivation. The innate immune response and NK-dependent IFN-secretion should be further investigated.


2004 ◽  
Vol 25 (6) ◽  
pp. 401-406 ◽  
Author(s):  
İrfan Kaygusuz ◽  
Ahmet Gödekmerdan ◽  
Erol Keleş ◽  
Turgut Karlidağ ◽  
Sinasi Yalçin ◽  
...  

1996 ◽  
Vol 11 (3) ◽  
pp. 474-480 ◽  
Author(s):  
C. Tzanno-Martins ◽  
L. S. Azevedo ◽  
N. Orii ◽  
E. Futata ◽  
V. Jorgetti ◽  
...  

2019 ◽  
Vol 115 (13) ◽  
pp. 1907-1917 ◽  
Author(s):  
Stefanie Finger ◽  
Maike Knorr ◽  
Michael Molitor ◽  
Rebecca Schüler ◽  
Venkata Garlapati ◽  
...  

Abstract Aims Myelomonocytic cells are critical in injury and healing post-myocardial infarction (MI). Mechanisms of regulation, however, are incompletely understood. The aim of the study was to elucidate the role of interferon gamma (IFN-γ) in the orchestrated inflammatory response in a murine model of MI. Methods and results MI was induced in 8- to 12-week-old male mice (C57BL/6 background) by permanent ligation of the left anterior descending (LAD) coronary artery. Lysozyme M (LysM)+ cell-depleted LysMiDTR transgenic mice displayed a reduced influx of CD45.2+/CD3−/CD11b+/Gr-1high neutrophils into infarcted myocardium 1 day post-MI compared with infarcted controls, paralleled by decreased cardiac mRNA levels of IFN-γ and tumour necrosis factor alpha (TNF-α). Mortality after MI was significantly increased in LysM+ cell-depleted mice within 28 days post-MI. To more specifically address the role of neutrophils, we depleted C57BL/6 mice with a monoclonal anti-Gr-1 antibody and found increased mortality, deteriorated cardiac function as well as decreased cardiac IFN-γ mRNA expression early after MI. Ccl2, Cxcl1, Cx3cl1, and Il12b mRNA were reduced 3 days after MI, as was the amount of CD11b+/Ly-6G−/Ly-6Chigh inflammatory monocytes. LAD-ligated Cramp−/− mice lacking cathelicidin important in neutrophil-dependent monocyte chemotaxis as well as IFNγ−/− and TNFα−/− mice phenocopied Gr-1+ cell-depleted mice, supporting a regulatory role of IFN-γ impacting on both the sequence of inflammatory cell invasion and cardiac outcome early after MI. The use of conditional IFN-γ receptor deficient mice indicated a direct effect of IFN-γ on LysM+ cells in cardiac injury post-MI. Using IFN-γ reporter mice and flow cytometry, we identified cardiac lymphoid cells (CD4+ and CD8+ T cells and natural killer cells) as primary source of this cytokine in the cardiac inflammatory response post-MI. Conclusion IFN-γ directs a sequential chemotactic cellular immune response and determines survival and cardiac function post-MI.


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