Chemoattractant Receptors Expressed on Type 2 T Cells and Their Role in Disease

2001 ◽  
Vol 125 (4) ◽  
pp. 273-279 ◽  
Author(s):  
Lorenzo Cosmi ◽  
Francesco Annunziato ◽  
Enrico Maggi ◽  
Sergio Romagnani ◽  
Roberto Manetti
Keyword(s):  
T Cells

Protection against autoimmune diabetes with oral insulin is associated with the presence of IL-4 type 2 T-cells in the pancreas and pancreatic lymph nodes

Diabetes ◽  
1998 ◽  
Vol 47 (1) ◽  
pp. 39-44 ◽  
Author(s):  
C. Ploix ◽  
I. Bergerot ◽  
N. Fabien ◽  
S. Perche ◽  
V. Moulin ◽  
...  
Keyword(s):  
T Cells ◽  
Lymph Nodes ◽  
Autoimmune Diabetes ◽  
Oral Insulin ◽  
Pancreatic Lymph Nodes

Identification of Helminth-induced Type 2 CD4+ T Cells and ILC2s

BIO-PROTOCOL ◽  
2014 ◽  
Vol 4 (11) ◽  
Author(s):  
Mario Zaiss ◽  
Kendle Maslowski
Keyword(s):  
T Cells ◽  
Cd4 T Cells

scholarly journals Potential Antiinflammatory Role of Insulin via the Preferential Polarization of Effector T Cells toward a T Helper 2 Phenotype

Endocrinology ◽  
2007 ◽  
Vol 148 (1) ◽  
pp. 346-353 ◽  
Author(s):  
Alexander Viardot ◽  
Shane T. Grey ◽  
Fabienne Mackay ◽  
Donald Chisholm
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Insulin Receptor ◽  
T Cell Differentiation ◽  
Receptor Expression ◽  
T Helper ◽  
Type Response ◽  
Helper Type

Hyperglycemia in critical illness is a common complication and a strong independent risk factor for morbidity and death. Intensive insulin therapy decreases this risk by up to 50%. It is unclear to what extent this benefit is due to reversal of glucotoxicity or to a direct effect of insulin, because antiinflammatory effects of insulin have already been described, but the underlying mechanisms are still poorly understood. The insulin receptor is expressed on resting neutrophils, monocytes, and B cells, but is not detectable on T cells. However, significant up-regulation of insulin receptor expression is observed on activated T cells, which suggests an important role during T cell activation. Exogenous insulin in vitro induced a shift in T cell differentiation toward a T helper type 2 (Th2)-type response, decreasing the T helper type 1 to Th2 ratio by 36%. This result correlated with a corresponding change in cytokine secretion, with the interferon-γ to IL-4 ratio being decreased by 33%. These changes were associated with increased Th2-promoting ERK phosphorylation in the presence of insulin. Thus, we demonstrate for the first time that insulin treatment influences T cell differentiation promoting a shift toward a Th2-type response. This effect of insulin in changing T cell polarization may contribute to its antiinflammatory role not only in sepsis, but also in chronic inflammation associated with obesity and type 2 diabetes.

scholarly journals Differential Activation of CD8+Tumor-Specific Tc1 and Tc2 Cells by an IL-10-Producing Murine Plasmacytoma

1998 ◽  
Vol 6 (3-4) ◽  
pp. 331-342 ◽  
Author(s):  
Christoph Specht ◽  
Hans-Gerd Pauels ◽  
Christian Becker ◽  
Eckehart Kölsch
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Tumor Cells ◽  
T Cell Subsets ◽  
Early Stages ◽  
Specific Tolerance

The involvement of counteractiveCD8+T-cell subsets during tumor-specific immune responses was analyzed in a syngeneic murine plasmacytoma model.CD8+Tc cells against the immunogenic IL-10-producing BALB/c plasmacytoma ADJ-PC-5 can be easily induced by immunization of BALB/c mice with X-irradiated ADJ-PC-5 tumor cellsin vivoandin vitro. However, the failure of recipient mice to mount a protective Tc response against the tumor during early stages of a real or simulated tumor growth is not due to immunological ignorance, but depends on the induction of tumor-specific tolerance, involving a population of tumorinducedCD8+T cells that are able to inhibit the generation of tumor-specific Tc cells in a primary ADJ-PC-5-specific MLTC, using IFN-γas a suppressive factor. Whereas most longterm cultivated CD8+ADJ-PC-5-specific Tc lines produce type-1 cytokines on stimulation, at least two of them, which were derived from a primary MLTC, display a type-2 cytokine spectrum. Furthermore, the primaryin vitroTc response against ADJ-PC-5 cells shows characteristics of a Tc2 response. The Tc response is strictly depending on tumor-derived IL-10.CD8+Tc cells that are induced in a primary MLTC do not produce IFN-γ, and the tumor-specific Tc response is enhanced by IL-4 but suppressed by IFN-γor IL-12. In contrast, ADJ-PC- 5-specificCD8+Tc cells from immunized mice are IFN-γproducing Tc1 cells. Since the primaryin vitroTc response against the tumor is suppressed even by the smallest numbers of irradiated ADJ-PC-5-specific Tc1 cells via IFN-γthese Tc1 cells behave similar to the suppressiveCD8+T cells that are induced during early stages of ADJ-PC-5 tumorigenesis.

scholarly journals A type 2 cytokine axis for thymus emigration

2017 ◽  
Vol 214 (8) ◽  
pp. 2205-2216 ◽  
Author(s):  
Andrea J. White ◽  
Song Baik ◽  
Sonia M. Parnell ◽  
Amanda M. Holland ◽  
Frank Brombacher ◽  
...  
Keyword(s):  
T Cells ◽  
Stromal Cells ◽  
Perivascular Spaces ◽  
Thymocyte Development ◽  
Invariant Nkt Cells ◽  
Developmental Program ◽  
Innate T Cells ◽  
Type 2 Cytokines ◽  
Thymic Stromal Cells

In the thymus, stromal microenvironments support a developmental program that generates mature T cells ready for thymic exit. The cellular and molecular specialization within thymic stromal cells that enables their regulation of specific stages of thymocyte development is poorly understood. Here, we show the thymic microenvironment expresses the type 2 IL-4R complex and is functionally responsive to its known ligands, IL-4 and IL-13. Absence of IL-4Rα limits thymocyte emigration, leading to an intrathymic accumulation of mature thymocytes within medullary perivascular spaces and reduced numbers of recent thymic emigrants. Thymus transplantation shows this requirement maps to IL-4Rα expression by stromal cells, and we provide evidence that it regulates thymic exit via a process distinct from S1P-mediated migration. Finally, we reveal a cellular mechanism by which IL-4+IL-13+ invariant NKT cells are necessary for IL-4Rα signaling that regulates thymic exit. Collectively, we define a new axis for thymic emigration involving stimulation of the thymic microenvironment via type 2 cytokines from innate T cells.

THU0007 Enhanced IGG4 Production by Follicular Helper Type 2 T Cells in IGG4-Related Disease

2016 ◽  
Vol 75 (Suppl 2) ◽  
pp. 180.1-180
Author(s):  
M. Akiyama ◽  
H. Yasuoka ◽  
K. Yamaoka ◽  
K. Suzuki ◽  
Y. Kaneko ◽  
...  
Keyword(s):  
T Cells ◽  
Related Disease ◽  
Igg4 Related Disease ◽  
Follicular Helper ◽  
Helper Type

Interactive effects of steroids and β-agonists on accumulation of type 2 T cells

2008 ◽  
Vol 121 (3) ◽  
pp. 750.e1-755.e3 ◽  
Author(s):  
Matthew J. Loza ◽  
Susan Foster ◽  
Stephen P. Peters ◽  
Raymond B. Penn
Keyword(s):  
T Cells ◽  
Interactive Effects

Strenuous exercise decreases the percentage of type 1 T cells in the circulation

2001 ◽  
Vol 91 (4) ◽  
pp. 1708-1712 ◽  
Author(s):  
Adam Steensberg ◽  
Anders Dyhr Toft ◽  
Helle Bruunsgaard ◽  
Marie Sandmand ◽  
Jens Halkjær-Kristensen ◽  
...  
Keyword(s):  
T Cells ◽  
Peak Plasma ◽  
Maximal Oxygen Consumption ◽  
Interferon Γ ◽  
Treadmill Running ◽  
Strenuous Exercise ◽  
Plasma Epinephrine ◽  
Lymphocyte Number

Prolonged strenuous exercise is followed by a temporary functional immune impairment. Low numbers of CD4+T helper (Th) and CD8+ T cytotoxic (Tc) cells are found in the circulation. These cells can be divided according to their cytokine profile into type 1 (Th1 and Tc1), which produce interferon-γ and interleukin (IL)-2, and type 2 (Th2 and Tc2) cells, which produce IL-4. The question addressed in the present study was whether exercise affected the relative balance between the circulating levels of these cytokine-producing T cells. Nine male runners performed treadmill running for 2.5 h at 75% of maximal oxygen consumption. The intracellular expression of cytokines was detected following stimulation with ionomycin and phorbol 12-myristate 13-acetate in blood obtained before, during, and after exercise. The percentage of type 1 T cells in the circulation was suppressed at the end of exercise and 2 h after exercise, whereas no changes were found in the percentage of type 2 T cells. Plasma epinephrine correlated negatively with the percentage of circulating CD8+ T cells producing IL-2, whereas peak IL-6 correlated with the percentage of CD8+ IL-4-producing T cells in the circulation. Peak plasma IL-6 correlated with plasma cortisol postrunning. In conclusion, the postexercise decrease in T lymphocyte number is accompanied by a more pronounced decrease in type 1 T cells, which may be linked to high plasma epinephrine. Furthermore, IL-6 may stimulate type 2 T cells, thereby maintaining a relatively unaltered percentage of these cells in the circulation compared with total circulating lymphocyte number.

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