Hypertrophy of infected Peyer's patches arises from global, interferon-receptor, and CD69-independent shutdown of lymphocyte egress

Schulz, Olga; Ugur, Milas; Friedrichsen, Michaela; Radulovic, Katarina; Niess, Jan Hendrik; Jalkanen, Sirpa; Krueger, Andreas; Pabst, Oliver

doi:10.1038/mi.2013.105

Cited by 22 publications

(36 citation statements)

References 49 publications

(131 reference statements)

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“…After FITC injection all cells inside the injected PP (PP inj ) were labelled as FITC þ cells 15 . Similar to the photoconversion method, we injected FITC into 4-5 PPs and the remaining non-injected PPs (PP ctrl ) served as internal controls.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, retention of recently activated T cells in lymphoid organs depends on CD69 (ref. 15). Since most of the resident CD4 þ T cells in PPs were CD69 hi , we hypothesized that CD69 might be involved in the retention of these cells in lymphoid tissues.…”

Section: Resultsmentioning

confidence: 99%

“…To generate H2B-Dendra2-expressing virus particles, MigH2BD2 (ref. 15) and pCL-Eco plasmids were transfected into HEK-293T cells using a calcium phosphate transfection kit (Invitrogen) and virus-containing supernatants were harvested. BM precursor cells were enriched by depleting lineage-committed cells using an antibody cocktail (CD11b, CD8b, CD49b, CD4, Gr-1, B220, CD11c and CD19) and Dynabeads (Invitrogen).…”

Section: Methodsmentioning

confidence: 99%

“…Thus, targeted illumination of cells that express such proteins allows spatiotemporal labelling of the cells. We developed two different methods by using either the photoconvertible protein Dendra2 or FITC injection to track effector/memory CD4 þ T cells in LNs and PPs 15 . Here, we describe a resident population of antigen-experienced CD4 þ T cells that resides in LNs and PPs for prolonged periods of time.…”

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confidence: 99%

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Resident CD4+ T cells accumulate in lymphoid organs after prolonged antigen exposure

et al. 2014

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Effector and memory CD4 þ T cells acquire distinct migratory properties depending on the type and location of the immune responses. Due to the highly dynamic nature of T cell circulation, the comprehensive analysis of these migratory routes requires dedicated experimental approaches. Here, we analyse the migration of effector/memory CD4 þ T cells by long-term in vivo cell tracking. We identify a resident population of antigen-experienced CD4 þ T cells that resides in lymph nodes and Peyer's patches without circulation or proliferation. Resident CD4 þ T cells constitute up to 50% of all effector/memory cells, including, but not limited to, follicular helper T cells. Furthermore, these non-circulating T cells possess a distinct T cell receptor repertoire and accumulate in Peyer's patches after continuous oral antigen exposure. Our results provide the first direct evidence for a resident population of effector/memory CD4 þ T cells that is retained in lymphoid tissues.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Resident CD4+ T cells accumulate in lymphoid organs after prolonged antigen exposure

et al. 2014

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“…To explore this idea, we quantified the recirculation rates of naive and memory B cells between PPs and spleen. To track B cell egress from PPs, we marked cells in situ in PPs by photoconversion as described 22,23 . We generated bone marrow-chimeric mice expressing the photoconvertible protein Dendra2 in hematopoietic cells (Dendra2 chimera).…”

Section: Memory Responses Generate Extraintestinal Plasma Cellsmentioning

confidence: 99%

Diversification of memory B cells drives the continuous adaptation of secretory antibodies to gut microbiota

Lindner¹,

Thomsen²,

Wahl³

et al. 2015

Nat Immunol

184

194

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Secretory immunoglobulin A (SIgA) shields the gut epithelium from luminal antigens and contributes to host-microbe symbiosis. However, how antibody responses are regulated to achieve sustained host-microbe interactions is unknown. We found that mice and humans exhibited longitudinal persistence of clonally related B cells in the IgA repertoire despite major changes in the microbiota during antibiotic treatment or infection. Memory B cells recirculated between inductive compartments and were clonally related to plasma cells in gut and mammary glands. Our findings suggest that continuous diversification of memory B cells constitutes a central process for establishing symbiotic host-microbe interactions and offer an explanation of how maternal antibodies are optimized throughout life to protect the newborn.

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CD69: from activation marker to metabolic gatekeeper

2017

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CD69 is a membrane-bound, type II C-lectin receptor. It is a classical early marker of lymphocyte activation due to its rapid appearance on the surface of the plasma membrane after stimulation. CD69 is expressed by several subsets of tissue resident immune cells, including resident memory T (TRM) cells and gamma delta (γδ) T cells, and is therefore considered a marker of tissue retention. Recent evidence has revealed that CD69 regulates some specific functions of selected T-cell subsets, determining the migrationretention ratio as well as the acquisition of effector or regulatory phenotypes. Specifically, CD69 regulates the differentiation of regulatory T (Treg) cells as well as the secretion of IFN-γ, IL-17, and IL-22. The identification of putative CD69 ligands, such as Galectin-1 (Gal-1), suggests that CD69-induced signaling can be regulated not only during cognate contacts between T cells and antigen-presenting cells in lymphoid organs, but also in the periphery, where cytokines and other metabolites control the final outcome of the immune response. Here, we will discuss new aspects of the molecular signaling mediated by CD69 and its involvement in the metabolic reprogramming regulating TH-effector lineages.Keywords: CD69 r Galectin-1 r LAT1 r Metabolism r mTOR r S1P1 r T cells IntroductionCD69 is a disulfide-linked homodimer protein with two differentially glycosylated subunits (28-32 kDa). Each subunit consists of an extracellular C-type lectin domain (CTLD) connected with a single-spanning transmembrane region followed by a short cytoplasmic tail (Fig. 1). The CD69 gene is located in the natural killer (NK) gene cluster, chromosome 6 in mouse and 12 in human [1,2]. Binding sites for several inducible transcriptional factors such as nuclear factor (NF)-κB, erythroblast transformationspecific related gene-1 (ERG-1) and activator protein-(AP-) 1 are located within the CD69 gene promoter [3,4]. CD69 expression is readily upregulated upon activation in most leukocytes, which underlies its widespread use as a marker of activated lymphocytes and NK cells, mainly [5]. In addition to its intrinsic value as an Correspondence: Dr. Francisco Sánchez-Madrid e-mail: fsmadrid@salud.madrid.org activation marker, recent evidence suggests that CD69 is also an important regulator of immune responses. Although the precise role of CD69 expression on immune cells function is yet to be elucidated, accumulating experimental evidence has revealed that CD69 may determine patterns of cytokine release as well as homing and migration of activated lymphocytes. In this review, we aim to update the state of the art regarding the functional role of CD69 in the regulation of the immune responses. We offer an integrated perspective of the mechanisms that drive the immune effects mediated by CD69 as well as potential synergies and antagonisms with other signaling routes involved in the immune response. CD69 is an early activation markerCD69 expression is rapidly induced on the surface of T lymphocytes after TCR/CD3 engagement, activating cy...

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Hypertrophy of infected Peyer's patches arises from global, interferon-receptor, and CD69-independent shutdown of lymphocyte egress

Cited by 22 publications

References 49 publications

Resident CD4+ T cells accumulate in lymphoid organs after prolonged antigen exposure

Resident CD4+ T cells accumulate in lymphoid organs after prolonged antigen exposure

Diversification of memory B cells drives the continuous adaptation of secretory antibodies to gut microbiota

CD69: from activation marker to metabolic gatekeeper

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