Aberrant B1?cell migration into the thymus results in activation of CD4 T?cells through its potent antigen-presenting activity in the development of murine lupus

2004 ◽  
Vol 34 (12) ◽  
pp. 3346-3358 ◽  
Author(s):  
Taku Sato ◽  
Sho Ishikawa ◽  
Kenji Akadegawa ◽  
Toshihiro Ito ◽  
Hideaki Yurino ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Migration ◽  
Cd4 T Cells ◽  
Murine Lupus ◽  
Antigen Presenting

scholarly journals Interleukin10-producing CD4 T cells ameliorate murine lupus in NZB/W F1 mice

2010 ◽  
Vol 69 (Suppl 2) ◽  
pp. A66-A66
Author(s):  
R Undeutsch ◽  
A Papendieck ◽  
J Y Humrich ◽  
G Riemekasten
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Murine Lupus

scholarly journals Regulatory CD4+ T Cells Promote B Cell Anergy in Murine Lupus

2014 ◽  
Vol 192 (9) ◽  
pp. 4069-4073 ◽  
Author(s):  
Yaoyang Liu ◽  
Aijing Liu ◽  
Noriko Iikuni ◽  
Huji Xu ◽  
Fu-Dong Shi ◽  
...  
Keyword(s):  
T Cells ◽  
B Cell ◽  
Cd4 T Cells ◽  
Murine Lupus ◽  
Cell Anergy ◽  
B Cell Anergy

scholarly journals Macrophage-dependent Apoptosis of CD4+ T Lymphocytes from HIV-infected Individuals Is Mediated by FasL and Tumor Necrosis Factor

1997 ◽  
Vol 185 (1) ◽  
pp. 55-64 ◽  
Author(s):  
Andrew D. Badley ◽  
David Dockrell ◽  
Margaret Simpson ◽  
Ron Schut ◽  
David H. Lynch ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
T Lymphocytes ◽  
Cd4 T Cells ◽  
Tumor Necrosis ◽  
Human Macrophages ◽  
Infected Cells ◽  
Induced Apoptosis ◽  
Antigen Presenting ◽  
Necrosis Factor

Apoptosis of bystander uninfected CD4+ T lymphocytes by neighboring HIV-infected cells is observed in cell culture and in lymphoid tissue of HIV-infected individuals. This study addresses whether antigen-presenting cells such as human macrophages mediate apoptosis of CD4+ T cells from HIV-infected individuals. Uninfected human macrophages, and to a larger degree, HIV-infected macrophages mediate apoptosis of T cells from HIV-infected, but not from uninfected control individuals. This macrophage-dependent killing targets CD4+, but not CD8+ T lymphocytes from HIV-infected individuals, and direct contact between macrophages and lymphocytes is required. Additional analyses indicated that the apoptosis-inducing ligands, FasL and tumor necrosis factor (TNF), mediate this macrophage-induced apoptosis of CD4+ T cells. These results support a role for macrophage-associated FasL and TNF in the selective depletion of CD4+ T cells in HIV-infected individuals.

scholarly journals Response of naive antigen-specific CD4+ T cells in vitro: characteristics and antigen-presenting cell requirements.

1992 ◽  
Vol 176 (5) ◽  
pp. 1431-1437 ◽  
Author(s):  
M Croft ◽  
D D Duncan ◽  
S L Swain
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Cd4 Cells ◽  
Peptide Antigen ◽  
Naive T Cells ◽  
Naïve T Cells ◽  
Antigen Presenting

Because of the low frequency of T cells for any particular soluble protein antigen in unprimed animals, the requirements for naive T cell responses in specific antigens have not been clearly delineated and they have been difficult to study in vitro. We have taken advantage of mice transgenic for the V beta 3/V alpha 11 T cell receptor (TCR), which can recognize a peptide of cytochrome c presented by IEk. 85-90% of CD4+ T cells in these mice express the transgenic TCR, and we show that almost all such V beta 3/V alpha 11 receptor-positive cells have a phenotype characteristic of naive T cells, including expression of high levels of CD45RB, high levels of L-selectin (Mel-14), low levels of CD44 (Pgp-1), and secretion of interleukin 2 (IL-2) as the major cytokine. Naive T cells, separated on the basis of CD45RB high expression, gave vigorous responses (proliferation and IL-2 secretion) to peptide antigen presented in vitro by a mixed antigen-presenting cell population. At least 50% of the T cell population appeared to respond, as assessed by blast transformation, entry into G1, and expression of increased levels of CD44 by 24 h. Significant contributions to the response by contaminating memory CD4+ cells were ruled out by demonstrating that the majority of the CD45RB low, L-selectin low, CD44 high cells did not express the V beta 3/V alpha 11 TCR and responded poorly to antigen. We find that proliferation and IL-2 secretion of the naive CD4 cells is minimal when resting B cells present peptide antigen, and that both splenic and bone marrow-derived macrophages are weak stimulators. Naive T cells did respond well to high numbers of activated B cells. However, dendritic cells were the most potent stimulators of proliferation and IL-2 secretion at low cell numbers, and were far superior inducers of IL-2 at higher numbers. These studies establish that naive CD4 T cells can respond vigorously to soluble antigen and indicate that maximal stimulation can be achieved by presentation of antigen on dendritic cells. This model should prove very useful in further investigations of activation requirements and functional characteristics of naive helper T cells.

scholarly journals Immune regulation of neuronal injury and repair by observing T cell activation

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Eric J. Regele ◽  
Elizabeth M. Runge ◽  
Felicia M. Kennedy ◽  
Virginia M. Sanders ◽  
Kathryn J. Jones
Keyword(s):  
T Cells ◽  
T Cell Activation ◽  
Cd4 T Cells ◽  
Cell Activation ◽  
Critical Role ◽  
Cd4 Cells ◽  
Knock Out ◽  
Facial Motoneuron ◽  
Injury And Repair ◽  
Antigen Presenting

Background and Hypothesis:  It is unknown how the immune system maintains the majority of facial motoneuron (FMN) survival after axotomy. IL-10 cytokine is necessary for FMN survival and CD4+ T cells are activated and play a critical role in survival, but do not produce IL-10. It was proposed that the source of IL-10 resides in the CNS; however, it is possible that antigen presenting cells (APC) produce IL-10 which activate CD4+ T cells to a neuroprotective phenotype. The regulation of IL-10 receptors (IL-10R) in immunodeficient compared to wild-type (WT) mice in the facial nucleus was studied in this experiment, as well as the possibility of the PNS producing IL-10.  Experimental Design or Project Methods:  To study APC’s role in motoneuron survival, we transferred WT whole splenocytes into global IL-10 knock out (KO) mice prior to axotomy. To study IL-10R gene expression, immunodeficient RAG-2 KO mice received WT or IL-10R-/- CD4+ T cells prior to axotomy.   Results:  qPCR revealed that WT mice upregulate IL-10R after axotomy, whereas RAG-2 KO mice had decreased expression comparatively. RAG-2 mice who received WT CD4+ T cells transfer restored IL-10R comparable to WT values.IL-10R was rescued in RAG-2 mice after the adoptive transfer of WT CD4+T cells. When IL-10R-/- CD4+ cells were transferred into RAG-2 mice, IL-10R values were restored; however, these T cells were unable to rescue FMN survival.   Conclusion and Potential Impact:  If WT whole splenocytes transferred into global IL-10 KO mice rescue FMN survival, it implies that APC play a role in producing IL-10. If they cannot mediate rescue, then peripheral IL-10 is unlikely sufficient for FMN survival. CD4+ T cells regulate central IL-10R response and must respond to IL-10 to mediate FMN survival. The transfer of whole splenocytes provides APCs capable of producing IL-10 and CD4+ T cells capable of responding to IL-10. 

scholarly journals Distinct Roles of α7 nAChRs in Antigen-Presenting Cells and CD4+ T Cells in the Regulation of T Cell Differentiation

2019 ◽  
Vol 10 ◽  
Author(s):  
Masato Mashimo ◽  
Masayo Komori ◽  
Yuriko Y. Matsui ◽  
Mami X. Murase ◽  
Takeshi Fujii ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Cd4 T Cells ◽  
Antigen Presenting Cells ◽  
T Cell Differentiation ◽  
Antigen Presenting ◽  
Α7 Nachrs

scholarly journals Interleukin (IL)-6 Directs the Differentiation of IL-4–producing CD4+ T Cells

1997 ◽  
Vol 185 (3) ◽  
pp. 461-470 ◽  
Author(s):  
Mercedes Rincón ◽  
Juan Anguita ◽  
Tetsuo Nakamura ◽  
Erol Fikrig ◽  
Richard A. Flavell
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Antigen Presenting Cells ◽  
Interferon Γ ◽  
T Helper Cell ◽  
Th2 Cells ◽  
T Helper ◽  
Key Factor ◽  
Antigen Presenting ◽  
Potent Factor

Interleukin (IL)-4 is the most potent factor that causes naive CD4+ T cells to differentiate to the T helper cell (Th) 2 phenotype, while IL-12 and interferon γ trigger the differentiation of Th1 cells. However, the source of the initial polarizing IL-4 remains unclear. Here, we show that IL-6, probably secreted by antigen-presenting cells, is able to polarize naive CD4+ T cells to effector Th2 cells by inducing the initial production of IL-4 in CD4+ T cells. These results show that the nature of the cytokine (IL-12 or IL-6), which is produced by antigen-presenting cells in response to a particular pathogen, is a key factor in determining the nature of the immune response.

scholarly journals Neuropilin-1 Expression on CD4 T Cells Is Atherogenic and Facilitates T Cell Migration to the Aorta in Atherosclerosis

2019 ◽  
Vol 203 (12) ◽  
pp. 3237-3246
Author(s):  
Dalia E. Gaddis ◽  
Lindsey E. Padgett ◽  
Runpei Wu ◽  
Catherine C. Hedrick
Keyword(s):  
T Cells ◽  
Cell Migration ◽  
T Cell ◽  
Cd4 T Cells ◽  
T Cell Migration ◽  
Neuropilin 1

scholarly journals CD4+ T-cell killing of multiple myeloma cells is mediated by resident bone marrow macrophages

2020 ◽  
Vol 4 (12) ◽  
pp. 2595-2605 ◽  
Author(s):  
Ole Audun W. Haabeth ◽  
Kjartan Hennig ◽  
Marte Fauskanger ◽  
Geir Åge Løset ◽  
Bjarne Bogen ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
T Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Antigen Presenting Cells ◽  
Bone Marrow Microenvironment ◽  
Cd4 T Cell ◽  
Myeloma Cells ◽  
Antigen Presenting

Abstract CD4+ T cells may induce potent antitumor immune responses through interaction with antigen-presenting cells within the tumor microenvironment. Using a murine model of multiple myeloma, we demonstrated that adoptive transfer of idiotype-specific CD4+ T cells may elicit curative responses against established multifocal myeloma in bone marrow. This finding indicates that the myeloma bone marrow niche contains antigen-presenting cells that may be rendered tumoricidal. Given the complexity of the bone marrow microenvironment, the mechanistic basis of such immunotherapeutic responses is not known. Through a functional characterization of antitumor CD4+ T-cell responses within the bone marrow microenvironment, we found that killing of myeloma cells is orchestrated by a population of bone marrow–resident CD11b+F4/80+MHC-IIHigh macrophages that have taken up and present secreted myeloma protein. The present results demonstrate the potential of resident macrophages as powerful mediators of tumor killing within the bone marrow and provide a basis for novel therapeutic strategies against multiple myeloma and other malignancies that affect the bone marrow.

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