P2X7R: The Achilles heel of follicular helper memory T cells

2020 ◽  
Vol 5 (45) ◽  
pp. eaba8097
Author(s):  
Jeffrey C. Nolz
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Memory T Cells ◽  
Related Research ◽  
Link Type ◽  
Follicular Helper ◽  
Research Article

Protecting TFH memory CD4+ T cells from NAD-induced cell death reveals both their longevity and plasticity (see related Research Article by Künzli et al.).

IFN-γ: The T cell’s license to kill stem cells in the inflamed intestine

2019 ◽  
Vol 4 (42) ◽  
pp. eaaz6821
Author(s):  
Kai Kretzschmar ◽  
Hans Clevers
Keyword(s):  
Stem Cells ◽  
T Cells ◽  
Cell Death ◽  
Stem Cell ◽  
Intestinal Injury ◽  
Intestinal Stem Cell ◽  
Related Research ◽  
Link Type ◽  
Research Article ◽  
Ifn Γ

IFN-γ produced by T cells directly induces intestinal stem cell death upon inflammation-induced intestinal injury (see the related Research Article byTakashimaet al.).

Tregs in fibrosis: To know your enemy, you must become your enemy

2019 ◽  
Vol 4 (39) ◽  
pp. eaay1160 ◽  
Author(s):  
Suzanne M. Bal ◽  
Ralph Stadhouders
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cytokine Production ◽  
T Helper ◽  
Related Research ◽  
T Helper 2 ◽  
Link Type ◽  
Research Article

T helper 2–skewed regulatory T cells in the skin use GATA3 to suppress local profibrotic type 2 cytokine production. See the related Research Article by Kalekar et al.

scholarly journals Lighting a fire on the reef

2020 ◽  
Vol 5 (54) ◽  
pp. eabf0905
Author(s):  
Zhibin Zhang ◽  
Judy Lieberman
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Caspase 3 ◽  
Bacterial Pathogen ◽  
Related Research ◽  
Link Type ◽  
Research Article

Coral gasdermin E is cleaved by activated caspase-3 to induce pyroptosis, a form of inflammatory programmed cell death, in response to a bacterial pathogen (see the related Research Article by Jiang et al.).

Myeloid cells in the central nervous system: So similar, yet so different

2019 ◽  
Vol 4 (32) ◽  
pp. eaaw2841 ◽  
Author(s):  
Francisco J. Quintana
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
Myeloid Cells ◽  
Related Research ◽  
Link Type ◽  
Research Article ◽  
The Central Nervous System

Dissection of the heterogeneity of CNS myeloid cells reveals functionally distinct subsets that govern encephalitogenic T cells. See related Research Article by Jordão et al.

scholarly journals Differential immune cell infiltrations between healthy periodontal and chronic periodontitis tissues

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Wei Li ◽  
Zheng Zhang ◽  
Zuo-min Wang
Keyword(s):  
T Cells ◽  
B Cells ◽  
Mast Cells ◽  
Plasma Cells ◽  
Immune Cell ◽  
Memory T Cells ◽  
Host Immunity ◽  
Memory B Cells ◽  
Helper T Cells ◽  
Follicular Helper

Abstract Background Host immunity plays an important role against oral microorganisms in periodontitis. Methods This study assessed the infiltrating immune cell subtypes in 133 healthy periodontal and 210 chronic periodontitis tissues from Gene Expression Omnibus (GEO) datasets using the CIBERSORT gene signature files. Results Plasma cells, naive B cells and neutrophils were all elevated in periodontitis tissues, when compared to those in healthy controls. In contrast, memory B cells, resting dendritic, mast cells and CD4 memory cells, as well as activated mast cells, M1 and M2 macrophages, and follicular helper T cells, were mainly present in healthy periodontal tissues. Furthermore, these periodontitis tissues generally contained a higher proportion of activated CD4 memory T cells, while the other subtypes of T cells, including resting CD4 memory T cells, CD8 T cells, follicular helper T cells (TFH) and regulatory T cells (Tregs), were relatively lower in periodontitis tissues, when compared to healthy tissues. The ratio of dendritic and mast cells and macrophages was lower in periodontitis tissues, when compared to healthy tissues. In addition, there was a significant negative association of plasma cells with most of the other immune cells, such as plasma cells vs. memory B cells (γ = − 0.84), plasma cells vs. resting dendritic cells (γ = − 0.64), plasma cells vs. resting CD4 memory T cells (γ = 0.50), plasma cells versus activated dendritic cells (γ = − 0.46), plasma cells versus TFH (γ = − 0.46), plasma cells versus macrophage M2 cells (γ = − 0.43), or plasma cells versus macrophage M1 cells (γ = − 0.40), between healthy control and periodontitis tissues. Conclusion Plasma cells, naive B cells and neutrophils were all elevated in periodontitis tissues. The infiltration of different immune cell subtypes in the periodontitis site could lead the host immunity against periodontitis.

Illuminating the core of adaptive immunity—how the regulatory genome controls Rag chromatin dynamics

2020 ◽  
Vol 5 (51) ◽  
pp. eabd6427
Author(s):  
Xun Wang ◽  
Ellen V. Rothenberg
Keyword(s):  
Adaptive Immunity ◽  
Large Scale ◽  
Chromatin Dynamics ◽  
Related Research ◽  
The Core ◽  
Link Type ◽  
Research Article ◽  
Super Enhancer ◽  
Regulatory Genome ◽  
Topological Changes

E2A specifies adaptive immunity by instructing large-scale topological changes for Rag gene super-enhancer formation (see the related Research Article by Miyazaki et al.).

scholarly journals Ddb1 Is Essential for the Expansion of CD4+ Helper T Cells by Regulating Cell Cycle Progression and Cell Death

2021 ◽  
Vol 12 ◽  
Author(s):  
Lingtao Yang ◽  
Wei Chen ◽  
Li Li ◽  
Yueyue Xiao ◽  
Shilin Fan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
Cell Death ◽  
Cell Cycle Progression ◽  
Helper T Cells ◽  
Genome Maintenance ◽  
Cycle Arrest ◽  
Follicular Helper ◽  
Acute Viral Infection ◽  
M Phase

Follicular helper T (TFH) cells are specialized CD4+ helper T cells that provide help to B cells in humoral immunity. However, the molecular mechanism underlying generation of TFH cells is incompletely understood. Here, we reported that Damage-specific DNA binding protein 1 (Ddb1) was required for expansion of CD4+ helper T cells including TFH and Th1 cells, germinal center response, and antibody response to acute viral infection. Ddb1 deficiency in activated CD4+ T cells resulted in cell cycle arrest at G2-M phase and increased cell death, due to accumulation of DNA damage and hyperactivation of ATM/ATR-Chk1 signaling. Moreover, mice with deletion of both Cul4a and Cul4b in activated CD4+ T cells phenocopied Ddb1-deficient mice, suggesting that E3 ligase-dependent function of Ddb1 was crucial for genome maintenance and helper T-cell generation. Therefore, our results indicate that Ddb1 is an essential positive regulator in the expansion of CD4+ helper T cells.

scholarly journals IL-4–Secreting Secondary T Follicular Helper (Tfh) Cells Arise from Memory T Cells, Not Persisting Tfh Cells, through a B Cell–Dependent Mechanism

2015 ◽  
Vol 194 (7) ◽  
pp. 2999-3010 ◽  
Author(s):  
Keke C. Fairfax ◽  
Bart Everts ◽  
Eyal Amiel ◽  
Amber M. Smith ◽  
Gabriele Schramm ◽  
...  
Keyword(s):  
T Cells ◽  
B Cell ◽  
Memory T Cells ◽  
Tfh Cells ◽  
Follicular Helper ◽  
Dependent Mechanism

Cutting down the hematopoietic tree: E-cadherin reveals a landscape of differentiating basophils and mast cells

2021 ◽  
Vol 6 (56) ◽  
pp. eabf7901
Author(s):  
Joakim S. Dahlin
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Related Research ◽  
Cell Lineages ◽  
Link Type ◽  
Research Article ◽  
E Cadherin

GATA-2–mediated E-cadherin expression marks early progenitors primed to the basophil and mast cell lineages in mouse hematopoiesis (see the related Research Article by Wanet et al.).

scholarly journals The relationship between CD4+ follicular helper T cells and CD8+ resident memory T cells: sisters or distant cousins?

2020 ◽  
Vol 32 (9) ◽  
pp. 583-587 ◽  
Author(s):  
Changwei Peng ◽  
Stephen C Jameson
Keyword(s):  
T Cells ◽  
Immune System ◽  
Protective Immunity ◽  
Memory T Cells ◽  
Helper T Cells ◽  
Lymphoid Tissues ◽  
Follicular Helper T Cells ◽  
Follicular Helper ◽  
Resident Memory T Cells ◽  
The Relationship

Abstract Independent studies over the last decade have characterized the properties of non-circulating CD8+ ‘resident’ memory T cells (TRM), which offer barrier protective immunity in non-lymphoid tissues and CD4+ follicular helper T cells (TFH), which mediate B-cell help in lymphoid sites. Despite their very different biological roles in the immune system, intriguing parallels have been noted between the trafficking properties and differentiation cues of these populations, parallels which have only sharpened with recent findings. In this review, we explore the features that underlie these similarities and discuss whether these indicate meaningful homologies in the development of CD8+ TRM and CD4+ TFH or reflect resemblances which are only ‘skin-deep’.

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