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Dear Colleagues,

Over the last few years, the research area of human immunology has been shaped by several novel concepts and technological advances, which have significantly contributed to translational progress in human health. Single-cell technologies, and most importantly, single-cell transcriptomics, have entered human immunology and provided more insights into the heterogeneity of lymphocyte populations, thus unmasking novel players in disease pathogenesis and their respective phenotypes, functions, and regulatory checkpoints.

Investigations in the area of human immunology have also shifted from the blood to the peripheral tissues. It has been acknowledged that 98% of human T cells reside in peripheral tissues, where they adapt to their local microenvironments and where they assume specialized functions. Their identity has been overlooked by a previous focus on the circulating blood compartment. We now consider these tissue-resident T cells (T_RM) to be critical for host defense, cancer, and autoimmunity. While great insights into T_RM cells in mouse models have been generated, insights into their identity in humans are just beginning to emerge. Considering their impact on human diseases, novel therapeutic strategies are expected to shape medicine in the near future.

While previous years of human T cell research have centered on T cell stability versus plasticity and on cytokine networks, we now consider T cells to be more malleable, with a multitude of external signals from the microenvironment. This includes not only their microbial antigens but also metabolites and even ionic signals.

All these taken together, human immunology has entered the center stage in translational research due to its great impact on human health and disease. This Special Issue invites you to share your expertise in this research topic.

Prof. Dr. Christina Zielinski
Guest Editor

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Related Special Issue

Published Papers (2 papers)

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Research

15 pages, 1416 KiB

Open AccessArticle

Peripheral Immunophenotype in IgG4-Related Disease and Its Association with Clinical Phenotypes and Disease Activity

by Eduardo Martín-Nares, Gabriela Hernández-Molina, Ángel A. Priego-Ranero, Isela Chan-Campos, Gladys S. Herrera-Noguera, Fidel López-Verdugo and Janette Furuzawa-Carballeda

Cells 2023, 12(4), 670; https://doi.org/10.3390/cells12040670 - 20 Feb 2023

Cited by 3 | Viewed by 2087

Abstract

Diverse immune cell subsets have been described in IgG4-related disease (IgG4-RD). If there is a different immunophenotype according to clinical phenotype and activity status is not known. Levels of IL-4-, IL-13-, IL-5-, and IL-21-producing CD4⁺ T cells (Th2 subsets), CD4⁺ cytotoxic T lymphocytes (CD4⁺CTLs), T helper 9 cells, T follicular helper cells (Tfh; Tfh1/Tfh2/Tfh17/Tf regulatory [Tfr]), Foxp3⁺ regulatory T cells, Type 1 regulatory T cells (Tr1), T helper 3 regulatory cells (Th3), IL-10-producing regulatory B cells (Bregs), IL-10-expressing regulatory plasmacytoid dendritic (pDC IL-10⁺) cells, and M1 and M2 monocytes were determined by flow cytometry in 43 IgG4-RD patients and 12 controls. All immune subsets were higher in patients vs. controls. CD4⁺/IL-4⁺, CD4⁺/IL-5⁺, CD4⁺CTLs, Tfh2, Tfh17, Tfr, and M1 monocyte cell number was different among IgG4-RD clinical phenotypes. The pancreato-hepato-biliary phenotype was characterized by a higher CD4⁺CTLs, Tfh17, Tfh2, and Tfr and lower M1 cell number. An increased CD4⁺CTLs and Th3 cell number distinguished the head and neck-limited phenotype, while the retroperitoneal/aortic and Mikulicz/systemic phenotypes were characterized by increased Th2 subsets. Tfh17, Tr1, Th3, pDC, M1, and M2 monocytes were augmented in active patients. In summary, the clinical heterogeneity of IgG4-RD might be driven by the participation of different immunophenotypes and, consequently, by a different fibroinflammatory process. Full article

(This article belongs to the Special Issue T Cell Responses in Human Health and Disease - Second Edition)

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13 pages, 4505 KiB

Open AccessArticle

Timing of Blood Sample Processing Affects the Transcriptomic and Epigenomic Profiles in CD4⁺ T-cells of Atopic Subjects

by Fahd Alhamdan, Kristina Laubhahn, Christine Happle, Anika Habener, Adan C. Jirmo, Clemens Thölken, Raffaele Conca, Ho-Ryun Chung, Gesine Hansen, Daniel P. Potaczek, Bianca Schaub, Ruth Grychtol and Holger Garn

Cells 2022, 11(19), 2958; https://doi.org/10.3390/cells11192958 - 22 Sep 2022

Cited by 1 | Viewed by 1732

Abstract

Optimal pre-analytical conditions for blood sample processing and isolation of selected cell populations for subsequent transcriptomic and epigenomic studies are required to obtain robust and reproducible results. This pilot study was conducted to investigate the potential effects of timing of CD4⁺ T-cell processing from peripheral blood of atopic and non-atopic adults on their transcriptomic and epigenetic profiles. Two heparinized blood samples were drawn from each of three atopic and three healthy individuals. For each individual, CD4⁺ T-cells were isolated from the first blood sample within 2 h (immediate) or from the second blood sample after 24 h storage (delayed). RNA sequencing (RNA-Seq) and histone H3K27 acetylation chromatin immunoprecipitation sequencing (ChIP-Seq) analyses were performed. A multiplicity of genes was shown to be differentially expressed in immediately processed CD4⁺ T-cells from atopic versus healthy subjects. These differences disappeared when comparing delayed processed cells due to a drastic change in expression levels of atopy-related genes in delayed processed CD4⁺ T-cells from atopic donors. This finding was further validated on the epigenomic level by examining H3K27 acetylation profiles. In contrast, transcriptomic and epigenomic profiles of blood CD4⁺ T-cells of healthy donors remained rather unaffected. Taken together, for successful transcriptomics and epigenomics studies, detailed standard operation procedures developed on the basis of samples from both healthy and disease conditions are implicitly recommended. Full article

(This article belongs to the Special Issue T Cell Responses in Human Health and Disease - Second Edition)

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