Characterization of IL-17-producing T helper cells-like autoreactive T cells          in aged mice

Abstract Objectives Preterm premature rupture of membranes (pPROM) causes preterm delivery, and increases maternal T-cell response against the fetus. Fetal inflammatory response prompts maturation of the newborn’s immunocompetent cells, and could be associated with unfavorable neonatal outcome. The aims were to examine the effects of pPROM (Mercer BM. Preterm premature rupture of the membranes: current approaches to evaluation and management. Obstet Gynecol Clin N Am 2005;32:411) on the newborn’s and mother’s immune system and (Test G, Levy A, Wiznitzer A, Mazor M, Holcberg G, Zlotnik A, et al. Factors affecting the latency period in patients with preterm premature rupture of membranes (pPROM). Arch Gynecol Obstet 2011;283:707–10) to assess the predictive value of immune system changes in neonatal morbidity. Methods Mother-newborn pairs (18 mothers and 23 newborns) who experienced pPROM and controls (11 mothers and 14 newborns), were enrolled. Maternal and neonatal whole blood samples underwent flow cytometry to measure lymphocyte subpopulations. Results pPROM-newborns had fewer naïve CD4 T-cells, and more memory CD4 T-cells than control newborns. The effect was the same for increasing pPROM latency times before delivery. Gestational age and birth weight influenced maturation of the newborns’ lymphocyte subpopulations and white blood cells, notably cytotoxic T-cells, regulatory T-cells, T-helper cells (absolute count), and CD4/CD8 ratio. Among morbidities, fewer naïve CD8 T-cells were found in bronchopulmonary dysplasia (BPD) (p=0.0009), and more T-helper cells in early onset sepsis (p=0.04). Conclusions pPROM prompts maturation of the newborn’s T-cell immune system secondary to antigenic stimulation, which correlates with pPROM latency. Maternal immunity to inflammatory conditions is associated with a decrease in non-major histocompatibility complex (MHC)-restricted cytotoxic cells.

Download Full-text

Generation of IL-8 and IL-9 Producing CD4+T Cells Is Affected by Th17 Polarizing Conditions and AHR Ligands

Mediators of Inflammation ◽

10.1155/2014/182549 ◽

2014 ◽

Vol 2014 ◽

pp. 1-14 ◽

Cited By ~ 13

Author(s):

Michaela Gasch ◽

Tina Goroll ◽

Mario Bauer ◽

Denise Hinz ◽

Nicole Schütze ◽

...

Keyword(s):

T Cells ◽

T Helper Cells ◽

Th17 Cells ◽

Immune Cell ◽

T Helper Cell ◽

Helper Cell ◽

T Helper ◽

Helper Cells ◽

Aryl Hydrocarbon

The T helper cell subsets Th1, Th2, Th17, and Treg play an important role in immune cell homeostasis, in host defense, and in immunological disorders. Recently, much attention has been paid to Th17 cells which seem to play an important role in the early phase of the adoptive immune response and autoimmune disease. When generating Th17 cells underin vitroconditions the amount of IL-17A producing cells hardly exceeds 20% while the nature of the remaining T cells is poorly characterized. As engagement of the aryl hydrocarbon receptor (AHR) has also been postulated to modulate the differentiation of T helper cells into Th17 cells with regard to the IL-17A expression we ask how far do Th17 polarizing conditions in combination with ligand induced AHR activation have an effect on the production of other T helper cell cytokines. We found that a high proportion of T helper cells cultured under Th17 polarizing conditions are IL-8 and IL-9 single producing cells and that AHR activation results in an upregulation of IL-8 and a downregulation of IL-9 production. Thus, we have identified IL-8 and IL-9 producing T helper cells which are subject to regulation by the engagement of the AHR.

Download Full-text

Functional and Chemical Characterization of B-Cell Growth Factor Produced by Normal Cloned T Helper Cells

Scandinavian Journal of Immunology ◽

10.1111/j.1365-3083.1984.tb00971.x ◽

1984 ◽

Vol 20 (1) ◽

pp. 7-14 ◽

Cited By ~ 3

Author(s):

S. PETTERSSON ◽

T. LEANDERSSON ◽

S. FORSGREN ◽

G. POBOR ◽

A. COUTINHO

Keyword(s):

Growth Factor ◽

Cell Growth ◽

B Cell ◽

T Helper Cells ◽

Chemical Characterization ◽

T Helper ◽

Helper Cells ◽

B Cell Growth Factor

Download Full-text

Changes in circulating Foxp3+regulatory T cells and interleukin-17-producing T helper cells during HBV-related acute-on-chronic liver failure

World Journal of Gastroenterology ◽

10.3748/wjg.v20.i26.8558 ◽

2014 ◽

Vol 20 (26) ◽

pp. 8558 ◽

Cited By ~ 15

Author(s):

Xue-Song Liang

Keyword(s):

T Cells ◽

Regulatory T Cells ◽

Liver Failure ◽

T Helper Cells ◽

Chronic Liver ◽

Interleukin 17 ◽

T Helper ◽

Chronic Liver Failure ◽

Helper Cells

Download Full-text

Role of accessory cells in cytokine production by T cells in chronic B- cell lymphocytic leukemia

Blood ◽

10.1182/blood.v86.3.1115.1115 ◽

1995 ◽

Vol 86 (3) ◽

pp. 1115-1123 ◽

Cited By ~ 31

Author(s):

T Decker ◽

T Flohr ◽

P Trautmann ◽

MJ Aman ◽

W Holter ◽

...

Keyword(s):

T Cells ◽

B Cell ◽

T Helper Cells ◽

Cytokine Production ◽

Lymphocytic Leukemia ◽

T Helper ◽

Ifn Gamma ◽

Helper Cells ◽

Accessory Cells ◽

Normal Individuals

Abstract We investigated the production of cytokines by highly purified T helper cells from B-cell chronic lymphocytic leukemia (B-CLL) patients stimulated by different activation pathways, and we studied the influence of various accessory cell populations on the pattern of the secretion of cytokines, including interleukin (IL)-2, IL-4, interferon- gamma (IFN-gamma), and IL-10. Neither a qualitative nor a quantitative difference in cytokine production and proliferative capacity was observed in CLL-derived purified T cells compared with normal individuals, when T cells were stimulated by different pathways, including CD3, CD2, and costimulation with CD28. Addition of autologous accessory cells (aAC), however, dramatically influenced the cytokine pattern of normal versus B-CLL-derived T cells. CLL cells as aAC caused a marked increase of IL-2, whereas IFN-gamma was only slightly induced and IL-4 was not influenced. In contrast, in normal individuals addition of aAC, which predominantly consisted of monocytes, resulted in a significant increase of IFN-gamma and a reduction of IL-4 secretion. IL-2 production was inhibited by higher concentrations of aAC. The increased stimulation of IL-2 production by CLL cells was not specific to the leukemic cell population, as purified B cells from normal individuals had the same effect. On the other hand, purified monocytes from CLL patients and controls both induced IFN-gamma production and inhibited IL-4 secretion. After antigen-specific stimulation with tetanus toxoid, cytokine secretion was influenced by the type of aAC in a similar pattern. We conclude that T helper cells derived from patients with B-CLL are intrinsically normal and that the predominance of B cells as accessory cells in CLL significantly alters the immune function of T helper cells in vitro.

Download Full-text

An idiotype-specific helper population that bears immunoglobulin, Ia, and Lyt-1 determinants.

Journal of Experimental Medicine ◽

10.1084/jem.159.4.1189 ◽

1984 ◽

Vol 159 (4) ◽

pp. 1189-1200 ◽

Cited By ~ 32

Author(s):

D H Sherr ◽

M E Dorf

Keyword(s):

T Cells ◽

B Cells ◽

Cell Population ◽

T Helper Cells ◽

T Helper ◽

Phenotypic Characteristics ◽

Surface Phenotype ◽

Specific Recognition ◽

Helper Cells ◽

Helper Activity

A helper cell population with phenotypic characteristics of both B and T cells is described. This helper population, called BH, is present in normal unprimed C57BL/6 mice and preferentially helps the expression of NPb idiotype-bearing plaque-forming B cells in the absence of T helper cells. Its surface phenotype is Lyt-1.2+, Ig+, Lyb-3+, Thy-1.2-, Lyt-2.2-. The helper activity of the BH population is IgH restricted and BH cells selectively bind NPb idiotypic determinants. Collectively the data demonstrate that this unique subpopulation can regulate the response of antibody-secreting B cells through specific recognition of idiotypic determinants.

Download Full-text

BATF is required for normal expression of gut-homing receptors by T helper cells in response to retinoic acid

Journal of Experimental Medicine ◽

10.1084/jem.20121088 ◽

2013 ◽

Vol 210 (3) ◽

pp. 475-489 ◽

Cited By ~ 35

Author(s):

Chuanwu Wang ◽

Shankar Thangamani ◽

Myunghoo Kim ◽

Bon-Hee Gu ◽

Jee H. Lee ◽

...

Keyword(s):

T Cells ◽

Retinoic Acid ◽

T Helper Cells ◽

Leucine Zipper ◽

Lymphocyte Activation ◽

T Helper ◽

Lymphocyte Migration ◽

Basic Leucine Zipper ◽

Helper Cells ◽

Normal Expression

CCR9 and α4β7 are the major trafficking receptors for lymphocyte migration to the gut, and their expression is induced during lymphocyte activation under the influence of retinoic acid (RA). We report here that BATF (basic leucine zipper transcription factor, ATF-like), an AP-1 protein family factor, is required for optimal expression of CCR9 and α4β7 by T helper cells. BATF-deficient (knockout [KO]) mice had reduced numbers of effector T and regulatory T cells in the intestine. The intestinal T cells in BATF KO mice expressed CCR9 and α4β7 at abnormally low levels compared with their wild-type (WT) counterparts, and BATF KO CD4+ T cells failed to up-regulate the expression of CCR9 and α4β7 to WT levels in response to RA. Defective binding of RARα and histone acetylation at the regulatory regions of the CCR9 and Itg-α4 genes were observed in BATF KO T cells. As a result, BATF KO effector and FoxP3+ T cells failed to populate the intestine, and neither population functioned normally in the induction and regulation of colitis. Our results establish BATF as a cellular factor required for normal expression of CCR9 and α4β7 and for the homeostasis and effector functions of T cell populations in the intestine.

Download Full-text