scholarly journals Characterization of HIV-induced remodeling reveals differences in infection susceptibility of memory CD4+ T cell subsets in vivo

Cell Reports ◽  
2021 ◽  
Vol 35 (4) ◽  
pp. 109038
Author(s):  
Guorui Xie ◽  
Xiaoyu Luo ◽  
Tongcui Ma ◽  
Julie Frouard ◽  
Jason Neidleman ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Subsets ◽  
Cd4 T Cell ◽  
Infection Susceptibility

scholarly journals Cd4+ T Cell Subsets during Virus Infection

2000 ◽  
Vol 191 (12) ◽  
pp. 2159-2170 ◽  
Author(s):  
Kevin J. Maloy ◽  
Christoph Burkhart ◽  
Tobias M. Junt ◽  
Bernhard Odermatt ◽  
Annette Oxenius ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Virus Infection ◽  
Cd4 T Cells ◽  
T Cell Subsets ◽  
Cd4 T Cell ◽  
Delayed Type Hypersensitivity ◽  
Protective Capacity ◽  
Peripheral Tissues

To analyze the antiviral protective capacities of CD4+ T helper (Th) cell subsets, we used transgenic T cells expressing an I-Ab–restricted T cell receptor specific for an epitope of vesicular stomatitis virus glycoprotein (VSV-G). After polarization into Th1 or Th2 effectors and adoptive transfer into T cell–deficient recipients, protective capacities were assessed after infection with different types of viruses expressing the VSV-G. Both Th1 and Th2 CD4+ T cells could transfer protection against systemic VSV infection, by stimulating the production of neutralizing immunoglobulin G antibodies. However, only Th1 CD4+ T cells were able to mediate protection against infection with recombinant vaccinia virus expressing the VSV-G (Vacc-IND-G). Similarly, only Th1 CD4+ T cells were able to rapidly eradicate Vacc-IND-G from peripheral organs, to mediate delayed-type hypersensitivity responses against VSV-G and to protect against lethal intranasal infection with VSV. Protective capacity correlated with the ability of Th1 CD4+ T cells to rapidly migrate to peripheral inflammatory sites in vivo and to respond to inflammatory chemokines that were induced after virus infection of peripheral tissues. Therefore, the antiviral protective capacity of a given CD4+ T cell is governed by the effector cytokines it produces and by its migratory capability.

Migration pathways of CD4 T cell subsets in vivo: the CD45RC- subset enters the thymus via α4 integrin-VCAM-1 interaction

1995 ◽  
Vol 7 (11) ◽  
pp. 1861-1871 ◽  
Author(s):  
Eric B. Bell ◽  
Sheila M. Sparshott ◽  
Ann Ager
Keyword(s):  
T Cell ◽  
T Cell Subsets ◽  
Cd4 T Cell ◽  
Migration Pathways

scholarly journals Characterization of CD4+ T cell subsets in allergy

2012 ◽  
Vol 24 (6) ◽  
pp. 700-706 ◽  
Author(s):  
Erik Wambre ◽  
Eddie A James ◽  
William W Kwok
Keyword(s):  
T Cell ◽  
T Cell Subsets ◽  
Cd4 T Cell

scholarly journals Characterization of mouse CD4 T cell subsets defined by expression of KLRG1

2007 ◽  
Vol 37 (12) ◽  
pp. 3445-3454 ◽  
Author(s):  
Niklas Beyersdorf ◽  
Xin Ding ◽  
Julia K. Tietze ◽  
Thomas Hanke
Keyword(s):  
T Cell ◽  
T Cell Subsets ◽  
Cd4 T Cell

scholarly journals Characterization of CD4+ T Cell Subsets in Patients with Abdominal Aortic Aneurysms

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Fábio Haach Téo ◽  
Rômulo Tadeu Dias de Oliveira ◽  
Liana Villarejos ◽  
Ronei Luciano Mamoni ◽  
Albina Altemani ◽  
...  
Keyword(s):  
T Cell ◽  
Mononuclear Cells ◽  
Aortic Aneurysms ◽  
T Cell Subsets ◽  
Cd4 T Cell ◽  
Peripheral Blood Mononuclear ◽  
Abdominal Aortic ◽  
Tissue Degradation

Background. The mediators produced by CD4+ T lymphocytes are involved in the pathogenesis of aneurysmal lesions in abdominal aortic aneurysm (AAA) patients. The aim of this study was to identify and characterize the CD4+ T cell subsets involved in human AAA. Methods. The CD4+ T cell subsets in 30 human aneurysmal lesions were determined using flow cytometry (FC) and immunohistochemistry (IHC). The peripheral blood mononuclear cells (PBMCs) from patients with AAA were also analyzed by FC and compared with control subjects. Results. Human aneurysmal lesions contained IFN-γ, IL-12p35, IL-4, IL-23p19, IL-17R, and IL-22 positive cells. PBMCs from AAA patients had higher expression levels of IFN-γ, TNF-α, IL-4, and IL-22 when compared to controls. Conclusions. Our results show the presence of TH1, TH2, TH17, and TH22 subsets in aneurysmal lesions of AAA patients and suggest that these cells may be mainly activated in situ, where they can induce tissue degradation and contribute to the pathogenesis of AAA.

scholarly journals Heterogeneity of the human CD4+ T-cell population: two distinct CD4+ T- cell subsets characterized by coexpression of CD45RA and CD45RO isoforms

Blood ◽  
1996 ◽  
Vol 88 (9) ◽  
pp. 3513-3521 ◽  
Author(s):  
D Hamann ◽  
PA Baars ◽  
B Hooibrink ◽  
RW van Lier
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Population ◽  
Intracellular Cytokine Staining ◽  
T Cell Subsets ◽  
Cd4 T Cell ◽  
Intermediate Phenotype ◽  
B Cell Differentiation ◽  
Gradual Loss

Activation of unprimed CD4+CD45RA+/RO- T-cells results in a gradual loss of CD45RA expression concomitant with the acquisition of CD45RO. It has been suggested that this conversion occurs in vivo through a CD45RAbright/RObright stage. Next to this small CD45RAbright/RObright subset (Dbright), a larger subpopulation that expresses both RA and RO isoforms at low levels (Ddull) can be found in the circulating CD4+ T-cell population of all donors. The properties of the latter population are largely undefined. Here, we show that Ddull cells have an intermediate phenotype for antigens such as CD31, CD621, CD58, and CD95 that are differentially expressed on unprimed versus primed T cells. In addition, they are able to provide help for B-cell differentiation and contain substantial numbers of tetanus toxoid (TT)-specific precursor cells. Remarkably, both intracellular cytokine staining and analysis of T-cell clones showed that Ddull cells and CD45RO+ T-cells produce comparable high amounts of both interferon (IFN)-gamma and interleukin (IL)-4, which clearly distinguishes them from CD45RA+ and Dbright T-cells. Finally, prolonged culture of sorted Ddull cells in a mixture of IL-2, IL-6, and tumor necrosis factor (TNF)-alpha showed that about half of the population retained the Ddull phenotype. Part of the cells upregulated the CD45RA isoform, whereas only a minority switched to single CD45RO expression. Our findings indicate that the Ddull population contains primed T cells, some of which may reacquire an “unprimed” phenotype in the absence of antigenic stimulation.

scholarly journals Lack of in vivo compartmentalization among HIV-1 infected naïve and memory CD4+ T cell subsets

Virology ◽  
2009 ◽  
Vol 393 (1) ◽  
pp. 24-32 ◽  
Author(s):  
Edwin J. Heeregrave ◽  
Mark J. Geels ◽  
Jason M. Brenchley ◽  
Elly Baan ◽  
David R. Ambrozak ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Subsets ◽  
Cd4 T Cell ◽  
Hiv 1

Role of Cytokines in the Differentiation of CD4+T-Cell Subsets in vivo

1991 ◽  
Vol 123 (1) ◽  
pp. 189-207 ◽  
Author(s):  
Robert L. Coffman ◽  
Kari Varkila ◽  
Phillip Scott ◽  
René Chatelain
Keyword(s):  
T Cell ◽  
T Cell Subsets ◽  
Cd4 T Cell

Characterization of CD4 + T cell subsets and HIV susceptibility in the inner and outer foreskin of Ugandan men

2019 ◽  
Vol 82 (1) ◽  
Author(s):  
Ronald Moses Galiwango ◽  
Sergey Yegorov ◽  
Vineet Joag ◽  
Jessica Prodger ◽  
Kamnoosh Shahabi ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Subsets ◽  
Cd4 T Cell ◽  
Hiv Susceptibility

scholarly journals The Role of CD4 T Cells in the Pathogenesis of Murine AIDS

2006 ◽  
Vol 80 (12) ◽  
pp. 5777-5789 ◽  
Author(s):  
Wen Li ◽  
William R. Green
Keyword(s):  
T Cells ◽  
T Cell ◽  
Nude Mice ◽  
Cd4 T Cells ◽  
T Regulatory Cells ◽  
T Cell Subsets ◽  
Cd4 T Cell ◽  
Regulatory Cells ◽  
Murine Aids

ABSTRACT LP-BM5, a retroviral isolate, induces a disease featuring retrovirus-induced immunodeficiency, designated murine AIDS (MAIDS). Many of the features of the LP-BM5-induced syndrome are shared with human immunodeficiency virus-induced disease. For example, CD4 T cells are critical to the development of MAIDS. In vivo depletion of CD4 T cells before LP-BM5 infection rendered genetically susceptible B6 mice MAIDS resistant. Similarly, MAIDS did not develop in B6.nude mice. However, if reconstituted with CD4 T cells, B6.nude mice develop full-blown MAIDS. Our laboratory has shown that the interaction of B and CD4 T cells that is central to MAIDS pathogenesis requires ligation of CD154 on CD4 T cells with CD40 on B cells. However, it is not clear which additional characteristics of the phenotypically and functionally heterogeneous CD4 T-cell compartment are required. Here, in vivo adoptive transfer experiments using B6.nude recipients are employed to compare the pathogenic abilities of CD4 T-cell subsets defined on the basis of cell surface phenotypic or functional differences. Th1 and Th2 CD4 T cells equally supported MAIDS induction. The rare Thy1.2 − CD4 subset that expands upon LP-BM5 infection was not necessary for MAIDS. Interestingly, CD45RBlow CD4 T cells supported significantly less disease than CD45RBhigh CD4 T cells. Because the decreased MAIDS pathogenesis could not be attributed to inhibition by CD45RBlow CD25+ natural T-regulatory cells, an intrinsic property of the CD45RBlow cells appeared responsible. Similarly, there was no evidence that natural T-regulatory cells played a role in LP-BM5-induced pathogenesis in the context of the intact CD4 T-cell population.

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