Presence of neutrophil-bearing antigen in lymphoid organs of immune mice

Blood ◽  
2006 ◽  
Vol 108 (9) ◽  
pp. 3094-3102 ◽  
Author(s):  
Belkys A. Maletto ◽  
Andrea S. Ropolo ◽  
Diego O. Alignani ◽  
Miriam V. Liscovsky ◽  
Romina P. Ranocchia ◽  
...  
Keyword(s):  
Immune Response ◽  
Lymphatic Vessels ◽  
Adaptive Immune Response ◽  
T Helper ◽  
T Helper 1 ◽  
Innate Response ◽  
Adaptive Immune ◽  
Tnf Α ◽  
New Evidence

Abstract Neutrophils play a crucial early role during the innate response, but little is known about their possible contribution when an adaptive immune response is installed. A robust neutrophilia and a T helper 1 (Th1) immune response are present after immunization with Complete Freund Adjuvant (CFA). We show that when FITC-labeled OVA was injected into the footpad of OVA/CFA immunized mice, the main OVA-FITC+ cells recruited in draining popliteal lymph nodes (LNs) were neutrophils, with most of them arriving at the LN by means of lymphatic vessels. The development of this OVA-FITC+ neutrophil influx requires an immune response against OVA. The OVA-FITC+ neutrophils present in LNs displayed mainly intracellular TNF-α, and their depletion resulted in an increase in the specific IL-5 levels. These data provide new evidence about the role played by neutrophils in vivo in adaptive immunity.

Late Breaking Abstract - Hypoxia dampens the allergen-dependent adaptive immune response and ameliorates allergic asthma in vivo

2021 ◽  
Author(s):  
Mathias Hochgerner ◽  
Eva M Sturm ◽  
Diana Schnoegl ◽  
Grazyna Kwapiszewska ◽  
Horst Olschewski ◽  
...  
Keyword(s):  
Immune Response ◽  
Allergic Asthma ◽  
Adaptive Immune Response ◽  
Adaptive Immune

scholarly journals An Exaggerated Monocyte-Derived Cytokine Response to Candida Hyphae in Patients With Recurrent Vulvovaginal Candidiasis

2020 ◽  
Author(s):  
Diletta Rosati ◽  
Mariolina Bruno ◽  
Martin Jaeger ◽  
Bart-Jan Kullberg ◽  
Frank van de Veerdonk ◽  
...  
Keyword(s):  
Immune Response ◽  
Mononuclear Cells ◽  
Cytokine Production ◽  
Adaptive Immune Response ◽  
Vulvovaginal Candidiasis ◽  
T Helper 1 ◽  
Recurrent Vulvovaginal Candidiasis ◽  
Tnf Α ◽  
Group A ◽  
Factor Α

Abstract Background Recurrent vulvovaginal candidiasis (RVVC) affects up to 8% of women. The immunopathogenesis is poorly understood but it has been suggested that RVVC might be due to dysregulated innate immune response. The aim of this study was to compare cytokine profiles in stimulated primary mononuclear cells (PBMCs) from RVVC and healthy individuals. Methods PBMCs isolated from RVVC patients (n = 24) and healthy volunteers (n = 30) were stimulated with unspecific and pathogen-specific antigens. Cytokine production was assessed after 24 hours, 48 hours, and 7 days using ELISA. Results No significant differences in cytokine production were found in T helper 1 (Th1), Th2, and Th17 immunity in response to both unspecific and pathogen-specific stimulations. Tumor necrosis factor-α (TNF-α) production in response to C. albicans hyphae was significantly higher in patients than controls and within the patient group, a significant positive correlation was found between interleukin-1β (IL-1β) and both TNF-α and IL-6. Both IL-1β/IL-1Ra and TNF-α/IL-10 ratios in Candida hyphae-stimulated PBMCs were significantly higher in patients than controls. Conclusions Women affected by RVVC showed increased monocytes-derived cytokine production, which might contribute to an exaggerated vaginal immune response to Candida hyphae. RVVC patients show no defective Th-dependent adaptive immune response upon Candida stimulation.

scholarly journals Consensus guidelines for the definition, detection and interpretation of immunogenic cell death

2020 ◽  
Vol 8 (1) ◽  
pp. e000337 ◽  
Author(s):  
Lorenzo Galluzzi ◽  
Ilio Vitale ◽  
Sarah Warren ◽  
Sandy Adjemian ◽  
Patrizia Agostinis ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Adaptive Immune Response ◽  
Operational Definition ◽  
Immunogenic Cell Death ◽  
Adaptive Immune ◽  
Regulated Cell Death ◽  
Definition Of

Cells succumbing to stress via regulated cell death (RCD) can initiate an adaptive immune response associated with immunological memory, provided they display sufficient antigenicity and adjuvanticity. Moreover, multiple intracellular and microenvironmental features determine the propensity of RCD to drive adaptive immunity. Here, we provide an updated operational definition of immunogenic cell death (ICD), discuss the key factors that dictate the ability of dying cells to drive an adaptive immune response, summarize experimental assays that are currently available for the assessment of ICD in vitro and in vivo, and formulate guidelines for their interpretation.

scholarly journals Polyphenol Effects on Splenic Cytokine Response in Post-Weaning Contactin 1-Overexpressing Transgenic Mice

Molecules ◽  
2019 ◽  
Vol 24 (12) ◽  
pp. 2205 ◽  
Author(s):  
Thea Magrone ◽  
Anna Spagnoletta ◽  
Antonella Bizzoca ◽  
Matteo Antonio Russo ◽  
Emilio Jirillo ◽  
...  
Keyword(s):  
Immune Response ◽  
Adaptive Immune Response ◽  
Immune Development ◽  
Adaptive Immune ◽  
Tnf Α ◽  
Pregnant Mice ◽  
Ifn Γ ◽  
Delayed Maturation ◽  
Red Grape ◽  
Necrosis Factor

Background: In mice, postnatal immune development has previously been investigated, and evidence of a delayed maturation of the adaptive immune response has been detected. Methods: In this study, the effects of red grape polyphenol oral administration on the murine immune response were explored using pregnant mice (TAG/F3 transgenic and wild type (wt) mice) as the animal model. The study was performed during pregnancy as well as during lactation until postnatal day 8. Suckling pups from polyphenol-administered dams as well as day 30 post-weaning pups (dietary-administered with polyphenols) were used. Polyphenol effects were evaluated, measuring splenic cytokine secretion. Results: Phorbol myristate acetate-activated splenocytes underwent the highest cytokine production at day 30 in both wt and TAG/F3 mice. In the latter, release of interferon (IFN)-γ and tumor necrosis factor (TNF)-α was found to be higher than in the wt counterpart. In this context, polyphenols exerted modulating activities on day 30 TAG/F3 mice, inducing release of interleukin (IL)-10 in hetero mice while abrogating release of IL-2, IFN-γ, TNF-α, IL-6, and IL-4 in homo and hetero mice. Conclusion: Polyphenols are able to prevent the development of an inflammatory/allergic profile in postnatal TAG/F3 mice.

scholarly journals Reduced Immune Response to Borrelia burgdorferi in the Absence of γδ T Cells

2011 ◽  
Vol 79 (10) ◽  
pp. 3940-3946 ◽  
Author(s):  
Cuixia Shi ◽  
Bikash Sahay ◽  
Jennifer Q. Russell ◽  
Karen A. Fortner ◽  
Nicholas Hardin ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Borrelia Burgdorferi ◽  
Adaptive Immune Response ◽  
Γδ T Cells ◽  
Content Type ◽  
Adaptive Immune ◽  
Cytokines And Chemokines

ABSTRACTLittle is known regarding the function of γδ T cells, although they accumulate at sites of inflammation in infections and autoimmune disorders. We previously observed that γδ T cellsin vitroare activated byBorrelia burgdorferiin a TLR2-dependent manner. We now observe that the activated γδ T cells can in turn stimulate dendritic cellsin vitroto produce cytokines and chemokines that are important for the adaptive immune response. This suggested thatin vivoγδ T cells may assist in activating the adaptive immune response. We examined this possibilityin vivoand observed that γδ T cells are activated and expand in number duringBorreliainfection, and this was reduced in the absence of TLR2. Furthermore, in the absence of γδ T cells, there was a significantly blunted response of adaptive immunity, as reflected in reduced expansion of T and B cells and reduced serum levels of anti-Borreliaantibodies, cytokines, and chemokines. This paralleled a greaterBorreliaburden in γδ-deficient mice as well as more cardiac inflammation. These findings are consistent with a model of γδ T cells functioning to promote the adaptive immune response during infection.

Interferon regulatory factor-1 is necessary for a T helper 1 immune response in vivo

1997 ◽  
Vol 56 ◽  
pp. 84
Author(s):  
M. Lohoff ◽  
D. Ferrick ◽  
H.-W. Mitrücker ◽  
G.S. Duncan ◽  
G.S. Duncan ◽  
...  
Keyword(s):  
Immune Response ◽  
Interferon Regulatory Factor ◽  
T Helper ◽  
Regulatory Factor ◽  
T Helper 1 ◽  
Interferon Regulatory Factor 1

scholarly journals A minimum of two distinct heritable factors are required to explain correlation structures in proliferating lymphocytes

2010 ◽  
Vol 7 (48) ◽  
pp. 1049-1059 ◽  
Author(s):  
John F. Markham ◽  
Cameron J. Wellard ◽  
Edwin D. Hawkins ◽  
Ken R. Duffy ◽  
Philip D. Hodgkin
Keyword(s):  
Flow Cytometry ◽  
Immune Response ◽  
Adaptive Immune Response ◽  
Time Lapse ◽  
Experimental Information ◽  
Flow Cytometry Data ◽  
Adaptive Immune ◽  
Three Phase

During the adaptive immune response, lymphocyte populations undergo a characteristic three-phase process: expansion through a series of cell divisions; cessation of expansion; and, finally, most of the accumulated lymphocytes die by apoptosis. The data used, thus far, to inform understanding of these processes, both in vitro and in vivo , are taken from flow cytometry experiments. One significant drawback of flow cytometry is that individual cells cannot be tracked, so that it is not possible to investigate interdependencies in the fate of cells within a family tree. This deficit in experimental information has recently been overcome by Hawkins et al . (Hawkins et al . 2009 Proc. Natl Acad. Sci. USA 106 , 13 457–13 462 ( doi:10.1073/pnas.0905629106 )), who reported on time-lapse microscopy experiments in which B-cells were stimulated through the TLR-9 receptor. Cells stimulated in this way do not aggregate, so that data regarding family trees can be recorded. In this article, we further investigate the Hawkins et al . data. Our conclusions are striking: in order to explain the familial correlation structure in division times, death times and propensity to divide, a minimum of two distinct heritable factors are necessary. As the data show that two distinct factors are necessary, we develop a stochastic model that has two heritable factors and demonstrate that it can reproduce the key features of the data. This model shows that two heritable factors are sufficient. These deductions have a clear impact upon biological understanding of the adaptive immune response. They also necessitate changes to the fundamental premises behind the tools developed by statisticians to draw deductions from flow cytometry data. Finally, they affect the mathematical modelling paradigms that are used to study these systems, as these are widely developed based on assumptions of cellular independence that are not accurate.

scholarly journals Mi-2β-targeted inhibition induces immunotherapy response in melanoma

2020 ◽  
Author(s):  
Bo Zhu ◽  
Zhengyu Wang ◽  
Licheng Yao ◽  
Xingyu Lin ◽  
Jie Zhang ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Checkpoint ◽  
Checkpoint Inhibitors ◽  
Adaptive Immune Response ◽  
Underlying Mechanism ◽  
Adaptive Immune ◽  
Melanoma Patients ◽  
Ifn Γ ◽  
Targeted Inhibition

Abstract Recent development of some new immune checkpoint inhibitors has been particularly successfully in melanoma, but the majority of melanoma patients exhibit resistance. Understanding and targeting the potential underlying mechanism/targets, especially the tumor-intrinsic modulators to convert resistant melanomas to immunotherapy sensitivity will potentially provide a significant improvement in patient outcome. Here, Mi-2β, a chromatin remodeling enzyme was identified as a key melanoma-intrinsic effector regulating the adaptive anti-tumor immune response. Loss of Mi-2β rescued the immune response to immunotherapy in vivo. Mechanistically, targeting Mi-2β induced the adaptive immune response by transcriptionally enhancing expression of a set of IFN-γ-responsive genes including CXCL9, CXCL10 and IRF1. Finally, we developed a Mi-2β-targeted inhibitor Z36-MP5, which specifically and effectively induced a response to immune checkpoint blockades in otherwise resistant melanomas. Our work provides a new insight into the epigenetic regulation in adaptive immune response, and highlights a viable strategy to improve immunotherapies in melanoma.

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