Adaptive and innate immune responses in MAC lung disease
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA819939 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18480900_1.fastq.gz | Fastqsanger.gz | |||
| SRR18480900_2.fastq.gz | Fastqsanger.gz | |||
| SRR18481000_1.fastq.gz | Fastqsanger.gz | |||
| SRR18481000_2.fastq.gz | Fastqsanger.gz | |||
| SRR18481100_1.fastq.gz | Fastqsanger.gz |
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Project description:Understanding the immune responses to SARS-CoV-2 vaccination is critical to optimizing vaccination strategies for individuals with autoimmune diseases, such as systemic lupus erythematosus (SLE). Here, we comprehensively analyzed innate and adaptive immune responses in 19 patients with SLE receiving a complete 2-dose Pfizer-BioNTech mRNA vaccine (BNT162b2) regimen compared with a control cohort of 56 healthy control (HC) volunteers. Patients with SLE exhibited impaired neutralizing antibody production and antigen-specific CD4+ and CD8+ T cell responses relative to HC. Interestingly, antibody responses were only altered in patients with SLE treated with immunosuppressive therapies, whereas impairment of antigen-specific CD4+ and CD8+ T cell numbers was independent of medication. Patients with SLE also displayed reduced levels of circulating CXC motif chemokine ligands, CXCL9, CXCL10, CXCL11, and IFN-γ after secondary vaccination as well as downregulation of gene expression pathways indicative of compromised innate immune responses. Single-cell RNA-Seq analysis reveals that patients with SLE showed reduced levels of a vaccine-inducible monocyte population characterized by overexpression of IFN-response transcription factors. Thus, although 2 doses of BNT162b2 induced relatively robust immune responses in patients with SLE, our data demonstrate impairment of both innate and adaptive immune responses relative to HC, highlighting a need for population-specific vaccination studies.
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Project description:CONTEXT Slowly progressive chronic tubulo-interstitial damage jeopardizes long-term renal allograft survival. Both immune and non-immune mechanisms are thought to contribute, but the most promising targets for timely intervention have not been identified. OBJECTIVE In the current study we seek to determine the driving force behind progressive histological damage of renal allografts, without the interference of donor pathology, delayed graft function and acute graft rejection. DESIGN We used microarrays to examine whole genome expression profiles in renal allograft protocol biopsies, and analyzed the correlation between gene expression and the histological appearance over time. The gene expression profiles in these protocol biopsies were then compared with gene expression of biopsies with acute T-cell mediated rejection. PATIENTS Human renal allograft biopsies (N=120) were included: 96 rejection-free protocol biopsies and 24 biopsies with T-cell mediated acute rejection. RESULTS In this highly cross-validated study, we demonstrate the significant association of established, ongoing and future chronic histological damage with regulation of adaptive immune gene expression (T-cell and B-cell transcript sets) and innate immune response gene expression (dendritic cell, NK-cell, mast cell and granulocyte transcripts). We demonstrate the ability of gene expression analysis to perform as a quantitative marker for ongoing inflammation with a wide dynamic range: from subtle subhistological inflammation prior to development of chronic damage, over moderate subclinical inflammation associated with chronic histological damage, to marked inflammation of Banff-grade acute T-cell mediated rejection. CONCLUSION Progressive chronic histological damage after kidney transplantation is associated with significant regulation of both innate and adaptive immune responses, months before the histological lesions appear. This study therefore corroborates the hypothesis that quantitative inflammation below the diagnostic threshold of classic T-cell or antibody-mediated rejection is associated with early subclinical stages of progressive renal allograft damage. We used microarrays to examine whole genome expression profiles in renal allograft protocol biopsies, and analyzed the correlation between gene expression and the histological appearance over time. The gene expression profiles in these protocol biopsies were then compared with gene expression of biopsies with acute T-cell mediated rejection. Human renal allograft biopsies (N=120) were included: 96 rejection-free protocol biopsies and 24 biopsies with T-cell mediated acute rejection.
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Project description:The immunological profile of patient-derived Precision Cut Tissue Slices (PCTS) obtained from neuroendocrine liver metastasis (LM-NEN=liver metastasis of neuroendocrine neoplasm) (n=3), cholangio carcinoma (CCA) (n=1) and tumour-free liver tissue (n=4) was analysed and the expression of 84 genes involved in innate and adaptive immune response was assessed. PCTS were kept in culture at 37C for 2 hours (recovery step) in a sealed chamber filled with carbogen under constant shaking prior to collection. Upon collection tissue slices were preserved in AllProtect Tissue Reagent (Qiagen) and stored at -80C until processing. RNA was isolated with Allprep Mini Kit (Qiagen) according to manifacturer's instructions. cDNA was synthesized with RT2 First Strand Kit (Qiagen) and analysed with Innate and Adaptive Immune Responses RT2 Profiler PCR Array (Qiagen) with RT2 SYBR® Green qPCR Mastermix (Qiagen). qPCR array for Human Innate & Adaptive Immune Responses (Qiagen 330231 PAHS-052ZA, full list of genes available online) was run on ABI 7500 Real-Time PCR System with an initial denaturation step at 95°C for 10 minutes followed by 40 cycles of denaturation at 95°C for 15 seconds and annealing/extension at 60°C for 60 seconds. More information about the histology of the slices used in this analysis can be found in the original manuscipt Doornebal et al.
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Project description:Miao2010 - Innate and adaptive immune
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This model is described in the article:
Quantifying the early immune
response and adaptive immune response kinetics in mice infected
with influenza A virus.
Miao H, Hollenbaugh JA, Zand MS,
Holden-Wiltse J, Mosmann TR, Perelson AS, Wu H, Topham DJ.
J. Virol. 2010 Jul; 84(13):
6687-6698
Abstract:
Seasonal and pandemic influenza A virus (IAV) continues to
be a public health threat. However, we lack a detailed and
quantitative understanding of the immune response kinetics to
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influence infection outcomes. To address these issues, we use
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developed to describe the dynamic interactions between target
(epithelial) cells, influenza virus, cytotoxic T lymphocytes
(CTLs), and virus-specific IgG and IgM. IAV and immune kinetic
parameters were estimated by fitting models to a large data set
obtained from primary H3N2 IAV infection of 340 mice. Prior to
a detectable virus-specific immune response (before day 5), the
estimated half-life of infected epithelial cells is
approximately 1.2 days, and the half-life of free infectious
IAV is approximately 4 h. During the adaptive immune response
(after day 5), the average half-life of infected epithelial
cells is approximately 0.5 days, and the average half-life of
free infectious virus is approximately 1.8 min. During the
adaptive phase, model fitting confirms that CD8(+) CTLs are
crucial for limiting infected cells, while virus-specific IgM
regulates free IAV levels. This may imply that CD4 T cells and
class-switched IgG antibodies are more relevant for generating
IAV-specific memory and preventing future infection via a more
rapid secondary immune response. Also, simulation studies were
performed to understand the relative contributions of
biological parameters to IAV clearance. This study provides a
basis to better understand and predict influenza virus
immunity.
This model is hosted on
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and identified by:
BIOMD0000000546.
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quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
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Project description:The relative contribution of innate and adaptive immunity to idiopathic inflammatory myopathy is poorly defined. We therefore sought to clarify these components of disease pathogenesis using our novel murine model of histidyl-tRNA synthetase (HRS)-induced myositis. Myositis was induced in WT and various congenic strains of C57BL/6 mice through intramuscular immunization with recombinant HRS. Histopathological, immunohistochemical, flow cytometric, and transcriptomic assessments were used to characterize muscle-infiltrating cell populations in these congenic strains. RAG1 KO mice developed markedly reduced muscle inflammation relative to WT mice, demonstrating a key requirement for T cells in driving HRS-induced myositis. Diminished cellular infiltration in CD4-Cre.MyD88fl/fl conditional knockout and OT-II TCR transgenic mice highlighted roles for innate and TCR-mediated/adaptive immune signaling in T cells. Transcriptionally-based pathway analyses showed that disruption of T cell signaling alters the function of macrophages, fibroblasts, and other non-lymphoid cell populations. Overall, these findings demonstrate that HRS-induced myositis reflects complex cellular interactions requiring the activation of both innate and adaptive T cell-mediated signaling pathways.
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