A robust platform for integrative spatial multi-omics analysis to map immune responses to SARS-CoV-2 infection in lung tissues
Immunology. 2023 Aug 21. doi: 10.1111/imm.13679. Online ahead of print.ABSTRACTThe SARS-CoV-2 (COVID-19) virus has caused a devastating global pandemic of respiratory illness. To understand viral pathogenesis, methods are available for studying dissociated cells in blood, nasal samples, bronchoalveolar lavage fluid and similar, but a robust platform for deep tissue characterization of molecular and cellular responses to virus infection in the lungs is still lacking. We developed an innovative spatial multi-omics platform to investigate COVID-19-infected lung tissues. Five tissue-profiling technologies were combined by a no...
Source: Immunology - August 22, 2023 Category: Allergy & Immunology Authors: Xiao Tan Laura F Grice Minh Tran Onkar Mulay James Monkman Tony Blick Tuan Vo Ana Clara Almeida Jarbas da Silva Motta Karen Fernandes de Moura Cleber Machado-Souza Paulo Souza-Fonseca-Guimaraes Cristina Pellegrino Baena Lucia de Noronha Fernanda Simoes Fo Source Type: research
TRAF5 regulates intestinal mucosal Th1/Th17 cell immune responses via Runx1 in colitis mice
Immunology. 2023 Aug 14. doi: 10.1111/imm.13685. Online ahead of print.ABSTRACTInflammatory bowel disease (IBD) is a chronic gastrointestinal inflammatory disease associated with CD4+ Th1 and Th17 cell immune responses. Tumour necrosis factor-associated factor 5 (TRAF5) deficiency has been shown to aggravate DSS-induced colitis. However, the potential role of TRAF5 in regulating CD4+ T cell immune responses in the pathogenesis of IBD remains unclear. TRAF5-/- CD4+ CD45RBhigh T cells and WT CD4+ CD45RBhigh T cells were transferred to Rag2-/- mice via intravenous (i.v.) tail injection, respectively, to establish a chronic co...
Source: Immunology - August 14, 2023 Category: Allergy & Immunology Authors: Mengting Li Caiqin Gan Runan Zhang Jiahui Wang Youwei Wang Weining Zhu Lan Liu Jian Shang Qiu Zhao Source Type: research
TRAF5 regulates intestinal mucosal Th1/Th17 cell immune responses via Runx1 in colitis mice
Immunology. 2023 Aug 14. doi: 10.1111/imm.13685. Online ahead of print.ABSTRACTInflammatory bowel disease (IBD) is a chronic gastrointestinal inflammatory disease associated with CD4+ Th1 and Th17 cell immune responses. Tumour necrosis factor-associated factor 5 (TRAF5) deficiency has been shown to aggravate DSS-induced colitis. However, the potential role of TRAF5 in regulating CD4+ T cell immune responses in the pathogenesis of IBD remains unclear. TRAF5-/- CD4+ CD45RBhigh T cells and WT CD4+ CD45RBhigh T cells were transferred to Rag2-/- mice via intravenous (i.v.) tail injection, respectively, to establish a chronic co...
Source: Immunology - August 14, 2023 Category: Allergy & Immunology Authors: Mengting Li Caiqin Gan Runan Zhang Jiahui Wang Youwei Wang Weining Zhu Lan Liu Jian Shang Qiu Zhao Source Type: research
TRAF5 regulates intestinal mucosal Th1/Th17 cell immune responses via Runx1 in colitis mice
Immunology. 2023 Aug 14. doi: 10.1111/imm.13685. Online ahead of print.ABSTRACTInflammatory bowel disease (IBD) is a chronic gastrointestinal inflammatory disease associated with CD4+ Th1 and Th17 cell immune responses. Tumour necrosis factor-associated factor 5 (TRAF5) deficiency has been shown to aggravate DSS-induced colitis. However, the potential role of TRAF5 in regulating CD4+ T cell immune responses in the pathogenesis of IBD remains unclear. TRAF5-/- CD4+ CD45RBhigh T cells and WT CD4+ CD45RBhigh T cells were transferred to Rag2-/- mice via intravenous (i.v.) tail injection, respectively, to establish a chronic co...
Source: Immunology - August 14, 2023 Category: Allergy & Immunology Authors: Mengting Li Caiqin Gan Runan Zhang Jiahui Wang Youwei Wang Weining Zhu Lan Liu Jian Shang Qiu Zhao Source Type: research
TRAF5 regulates intestinal mucosal Th1/Th17 cell immune responses via Runx1 in colitis mice
Immunology. 2023 Aug 14. doi: 10.1111/imm.13685. Online ahead of print.ABSTRACTInflammatory bowel disease (IBD) is a chronic gastrointestinal inflammatory disease associated with CD4+ Th1 and Th17 cell immune responses. Tumour necrosis factor-associated factor 5 (TRAF5) deficiency has been shown to aggravate DSS-induced colitis. However, the potential role of TRAF5 in regulating CD4+ T cell immune responses in the pathogenesis of IBD remains unclear. TRAF5-/- CD4+ CD45RBhigh T cells and WT CD4+ CD45RBhigh T cells were transferred to Rag2-/- mice via intravenous (i.v.) tail injection, respectively, to establish a chronic co...
Source: Immunology - August 14, 2023 Category: Allergy & Immunology Authors: Mengting Li Caiqin Gan Runan Zhang Jiahui Wang Youwei Wang Weining Zhu Lan Liu Jian Shang Qiu Zhao Source Type: research
TRAF5 regulates intestinal mucosal Th1/Th17 cell immune responses via Runx1 in colitis mice
Immunology. 2023 Aug 14. doi: 10.1111/imm.13685. Online ahead of print.ABSTRACTInflammatory bowel disease (IBD) is a chronic gastrointestinal inflammatory disease associated with CD4+ Th1 and Th17 cell immune responses. Tumour necrosis factor-associated factor 5 (TRAF5) deficiency has been shown to aggravate DSS-induced colitis. However, the potential role of TRAF5 in regulating CD4+ T cell immune responses in the pathogenesis of IBD remains unclear. TRAF5-/- CD4+ CD45RBhigh T cells and WT CD4+ CD45RBhigh T cells were transferred to Rag2-/- mice via intravenous (i.v.) tail injection, respectively, to establish a chronic co...
Source: Immunology - August 14, 2023 Category: Allergy & Immunology Authors: Mengting Li Caiqin Gan Runan Zhang Jiahui Wang Youwei Wang Weining Zhu Lan Liu Jian Shang Qiu Zhao Source Type: research
Inhibition of PI3K p110 δ activity reduces IgE production in IL-4 and anti-CD40 stimulated human B cell cultures
In conclusion, PI3K p110δ signalling is required for the production of human IgE, which makes it a pharmacological target for the treatment of allergic disease.PMID:37530226 | DOI:10.1111/imm.13684 (Source: Immunology)
Source: Immunology - August 2, 2023 Category: Allergy & Immunology Authors: Anna Cutrina-Pons Aloka De Sa David J Fear Hannah J Gould Faruk Ramadani Source Type: research
Inhibition of PI3K p110 δ activity reduces IgE production in IL-4 and anti-CD40 stimulated human B cell cultures
In conclusion, PI3K p110δ signalling is required for the production of human IgE, which makes it a pharmacological target for the treatment of allergic disease.PMID:37530226 | DOI:10.1111/imm.13684 (Source: Immunology)
Source: Immunology - August 2, 2023 Category: Allergy & Immunology Authors: Anna Cutrina-Pons Aloka De Sa David J Fear Hannah J Gould Faruk Ramadani Source Type: research
Inhibition of PI3K p110 δ activity reduces IgE production in IL-4 and anti-CD40 stimulated human B cell cultures
In conclusion, PI3K p110δ signalling is required for the production of human IgE, which makes it a pharmacological target for the treatment of allergic disease.PMID:37530226 | DOI:10.1111/imm.13684 (Source: Immunology)
Source: Immunology - August 2, 2023 Category: Allergy & Immunology Authors: Anna Cutrina-Pons Aloka De Sa David J Fear Hannah J Gould Faruk Ramadani Source Type: research
Inhibition of PI3K p110 δ activity reduces IgE production in IL-4 and anti-CD40 stimulated human B cell cultures
In conclusion, PI3K p110δ signalling is required for the production of human IgE, which makes it a pharmacological target for the treatment of allergic disease.PMID:37530226 | DOI:10.1111/imm.13684 (Source: Immunology)
Source: Immunology - August 2, 2023 Category: Allergy & Immunology Authors: Anna Cutrina-Pons Aloka De Sa David J Fear Hannah J Gould Faruk Ramadani Source Type: research
Inhibition of PI3K p110 δ activity reduces IgE production in IL-4 and anti-CD40 stimulated human B cell cultures
In conclusion, PI3K p110δ signalling is required for the production of human IgE, which makes it a pharmacological target for the treatment of allergic disease.PMID:37530226 | DOI:10.1111/imm.13684 (Source: Immunology)
Source: Immunology - August 2, 2023 Category: Allergy & Immunology Authors: Anna Cutrina-Pons Aloka De Sa David J Fear Hannah J Gould Faruk Ramadani Source Type: research
Inhibition of PI3K p110 δ activity reduces IgE production in IL-4 and anti-CD40 stimulated human B cell cultures
In conclusion, PI3K p110δ signalling is required for the production of human IgE, which makes it a pharmacological target for the treatment of allergic disease.PMID:37530226 | DOI:10.1111/imm.13684 (Source: Immunology)
Source: Immunology - August 2, 2023 Category: Allergy & Immunology Authors: Anna Cutrina-Pons Aloka De Sa David J Fear Hannah J Gould Faruk Ramadani Source Type: research
Inhibition of PI3K p110 δ activity reduces IgE production in IL-4 and anti-CD40 stimulated human B cell cultures
In conclusion, PI3K p110δ signalling is required for the production of human IgE, which makes it a pharmacological target for the treatment of allergic disease.PMID:37530226 | DOI:10.1111/imm.13684 (Source: Immunology)
Source: Immunology - August 2, 2023 Category: Allergy & Immunology Authors: Anna Cutrina-Pons Aloka De Sa David J Fear Hannah J Gould Faruk Ramadani Source Type: research
Inhibition of PI3K p110 δ activity reduces IgE production in IL-4 and anti-CD40 stimulated human B cell cultures
In conclusion, PI3K p110δ signalling is required for the production of human IgE, which makes it a pharmacological target for the treatment of allergic disease.PMID:37530226 | DOI:10.1111/imm.13684 (Source: Immunology)
Source: Immunology - August 2, 2023 Category: Allergy & Immunology Authors: Anna Cutrina-Pons Aloka De Sa David J Fear Hannah J Gould Faruk Ramadani Source Type: research
Inhibition of PI3K p110 δ activity reduces IgE production in IL-4 and anti-CD40 stimulated human B cell cultures
In conclusion, PI3K p110δ signalling is required for the production of human IgE, which makes it a pharmacological target for the treatment of allergic disease.PMID:37530226 | DOI:10.1111/imm.13684 (Source: Immunology)
Source: Immunology - August 2, 2023 Category: Allergy & Immunology Authors: Anna Cutrina-Pons Aloka De Sa David J Fear Hannah J Gould Faruk Ramadani Source Type: research
