scholarly journals Circulating Th1 and Th2 cytokines in patients with hepatitis C virus infection

1998 ◽  
Vol 7 (4) ◽  
pp. 295-297 ◽  
Author(s):  
X. G. Fan ◽  
W. E. Liu ◽  
C. Z. Li ◽  
Z. C. Wang ◽  
L. X. Luo ◽  
...  
Keyword(s):  
Hcv Infection ◽  
Th2 Cytokines ◽  
Th1 And Th2 Cytokines ◽  
Th1 Cytokine ◽  
Chronic Hcv Infection ◽  
Ifn Γ ◽  
Chronic Hcv ◽  
Th1 Cytokines ◽  
Normal Controls ◽  
Th1 And Th2

The imbalance of T-helper (Th) lymphocyte cytokine production may play an important role in immunopathogenes is of persistent hepatitis C virus (HCV) infection. To know whether an imbalance between Th1 and Th2 cytokines is present in chronic HCV infection, serum levels of Th1 cytokines , interferon gamma (IFN-γ ) and interleukin (IL)-2, and Th2 cytokines, IL-4 and IL-10, were measured using enzyme - linked immunosorbent as say in this study. Eighteen individuals with chronic HCV infection, 11 healthy subjects as normal controls and 10 chronic HBV infected patients as disease controls were observed. The results showed that the leve ls of Th2 cytokines (IL-4 and IL-10) were significantly increased inchronic HCV infected patients compared with normal controls (IL-4: 30.49 ± 17.55 vs . 14.94 ± 13.73, pg/ml,p<0.025; IL-10: 50.30 ± 19.59 vs. 17.87 ± 9.49, pg/ml,p<0.001). Similarly, the levels of Th1 cytokine, IL-2, was also elevated in individuals with chronic HCV infection when compared with normal controls (IL-2: 118.53 ± 95.23 vs . 61.57 ± 28.70, pg/ml,p<0.05). However, Th1 cytokine IFN-γ level was not significantly changed during HCV infection (IFN-γ: 28.09 ± 15.65 vs . 24.10 ± 15.61, pg/ml,p>0.05). Further more, the elevated levels of Th2 cytokines are greater than Th1 cytokines in HCV infection. Thus , the study indicates that an enhanced Th2 responses are present during chronic HCV infection, which may partly be responsible for the persistence of HCV infection.

scholarly journals Role of Th1 and Th2 Cytokines in Immune Response to Uncomplicated Plasmodium falciparum Malaria

2002 ◽  
Vol 9 (2) ◽  
pp. 348-351 ◽  
Author(s):  
Donato Torre ◽  
Filippo Speranza ◽  
Massimo Giola ◽  
Alberto Matteelli ◽  
Roberto Tambini ◽  
...  
Keyword(s):  
Immune Response ◽  
Plasmodium Falciparum ◽  
Interleukin 12 ◽  
Th2 Cytokines ◽  
Th1 And Th2 Cytokines ◽  
Ifn Γ ◽  
Anti Inflammatory ◽  
Th1 Cytokines ◽  
Th1 And Th2

ABSTRACT The relative balance between Th1 and Th2 cytokines appears crucial, since the role of cytokines has been evaluated in several studies by comparison of clinically heterogeneous groups of patients. The aim of this study is to determine the role of proinflammatory Th1 cytokines, interleukin-12 (IL-12) and gamma interferon (IFN-γ), and anti-inflammatory Th2 cytokines, IL-4 and IL-10, in a homogeneous group of patients with uncomplicated Plasmodium falciparum malaria. Levels of IL-12, IFN-γ, Il-4, and IL-10 in serum for 20 adult patients and 15 healthy control subjects were determined by an immunoenzymatic assay. Serum levels of Th1 cytokines, IL-12 (8.6 ± 2.8 pg/ml; controls, 3.2 ± 0.7 pg/ml) and IFN-γ (39.2 ± 67.6 pg/ml; controls, 8.4 ± 6.3 pg/ml), were significantly increased at admission; 3 days later, levels of IL-12 in serum remained significantly high (8.8 ± 2.6 pg/ml), whereas IFN-γ levels returned to control values. The anti-inflammatory response of Th2 cytokines (IL-10 and IL-4) was distinct. Levels of IL-10 in serum were not significantly increased at day 0 and day 3 (306.6 ± 200.4 pg/ml and 56.6 ± 38.4 pg/ml, respectively; controls, 17.4 ± 9.0 pg/ml). In contrast, levels of IL-4 in serum were not increased on admission (3.4 ± 1.2 pg/ml; controls, 2.4 ± 0.8 pg/ml), but at day 3 a moderate and significant increase of IL-4 levels was observed (4.5 ± 1.7 pg/ml). In conclusion, the increase of Th1 cytokine IL-12 and IFN-γ levels during the acute phase of uncomplicated P. falciparum malaria may reflect an early and effective immune response regulated by proinflammatory Th1 cytokines, and in particular IFN-γ may play a role in limiting progression from uncomplicated malaria to severe and life-threatening complications.

scholarly journals The Th1 and Th2 cytokines IFN-γ and IL-4 antagonize the inhibition of monocyte IL-1 receptor antagonist by glucocorticoids: involvement of IL-1

1998 ◽  
Vol 28 (7) ◽  
pp. 2075-2085 ◽  
Author(s):  
Damián Kovalovsky ◽  
Marcelo Páez Pereda ◽  
Joachim Sauer ◽  
Carolina Perez Castro ◽  
Victor E. Nahmod ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Th2 Cytokines ◽  
Th1 And Th2 Cytokines ◽  
Ifn Γ ◽  
Th1 And Th2

scholarly journals Modulation of Helper T Cytokines in Thymus during Early Pregnancy in Ewes

Animals ◽  
2019 ◽  
Vol 9 (5) ◽  
pp. 245 ◽  
Author(s):  
Leying Zhang ◽  
Zimo Zhao ◽  
Hao Mi ◽  
Baoliang Liu ◽  
Bin Wang ◽  
...  
Keyword(s):  
Immune System ◽  
Estrous Cycle ◽  
Early Pregnancy ◽  
Interleukin 2 ◽  
Th2 Cytokines ◽  
Maternal Immune System ◽  
Th1 And Th2 Cytokines ◽  
Ifn Γ ◽  
Necrosis Factor ◽  
Th1 And Th2

There is an immune tolerance in maternal immune system during pregnancy, and thymus is a main organ of the immune system. Helper T (Th)1 and Th2 cytokines are involved in the regulation of immune system, but the modulation of Th cytokines in the thymus during early pregnancy is unclear in ewes. Thymuses were collected on day 16 of the estrous cycle, and on days 13, 16, and 25 of pregnancy in ewes. qRT-PCR, Western blot, and immunohistochemistry were used to analyze the expression of Th1 and Th2 cytokines in the thymuses. There was a peak in the expression of interferon-gamma (IFN-γ) on day 16 of pregnancy, an upregulation of tumor necrosis factor beta (TNF-β), and a sustained expression of interleukin-2 (IL-2) and IL-4. Furthermore, there was a peak in the expression of IL-6 on day 13 of pregnancy, no expression of IL-6 on day 16 of the estrous cycle and day 25 of pregnancy, and an upregulation of IL-5 and IL-10 in the thymuses during early pregnancy. The immunohistochemistry results revealed that the IFN-γ and IL-6 proteins were limited to the stromal cells, capillaries, and thymic corpuscles. In conclusion, early pregnancy influenced the production of Th1 and Th2 cytokines of maternal thymus in sheep.

scholarly journals Chronic Hepatitis C Virus Infection Impairs M1 Macrophage Differentiation and Contributes to CD8+ T-Cell Dysfunction

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 374 ◽  
Author(s):  
Faria Ahmed ◽  
Andrea Ibrahim ◽  
Curtis L. Cooper ◽  
Ashok Kumar ◽  
Angela M. Crawley
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Cd8 T Cell ◽  
Hcv Infection ◽  
M1 Macrophage ◽  
T Cell Dysfunction ◽  
Chronic Hcv Infection ◽  
Ifn Γ ◽  
Chronic Hcv

Chronic hepatitis C virus (HCV) infection causes generalized CD8+ T cell impairment, not limited to HCV-specific CD8+ T-cells. Liver-infiltrating monocyte-derived macrophages (MDMs) contribute to the local micro-environment and can interact with and influence cells routinely trafficking through the liver, including CD8+ T-cells. MDMs can be polarized into M1 (classically activated) and M2a, M2b, and M2c (alternatively activated) phenotypes that perform pro- and anti-inflammatory functions, respectively. The impact of chronic HCV infection on MDM subset functions is not known. Our results show that M1 cells generated from chronic HCV patients acquire M2 characteristics, such as increased CD86 expression and IL-10 secretion, compared to uninfected controls. In contrast, M2 subsets from HCV-infected individuals acquired M1-like features by secreting more IL-12 and IFN-γ. The severity of liver disease was also associated with altered macrophage subset differentiation. In co-cultures with autologous CD8+ T-cells from controls, M1 macrophages alone significantly increased CD8+ T cell IFN-γ expression in a cytokine-independent and cell-contact-dependent manner. However, M1 macrophages from HCV-infected individuals significantly decreased IFN-γ expression in CD8+ T-cells. Therefore, altered M1 macrophage differentiation in chronic HCV infection may contribute to observed CD8+ T-cell dysfunction. Understanding the immunological perturbations in chronic HCV infection will lead to the identification of therapeutic targets to restore immune function in HCV+ individuals, and aid in the mitigation of associated negative clinical outcomes.

P.200 Comprehensive analysis of IFN-γ and IL-2 production by T cells in acute and chronic HCV infection

2006 ◽  
Vol 36 ◽  
pp. S123
Author(s):  
R.A. Ffrench ◽  
J. Flynn ◽  
K. Goy ◽  
P. Hosseiny ◽  
Y. Pan ◽  
...  
Keyword(s):  
T Cells ◽  
Comprehensive Analysis ◽  
Hcv Infection ◽  
Chronic Hcv Infection ◽  
Ifn Γ ◽  
Chronic Hcv

scholarly journals Th2 Cytokine Levels Distort the Association of IL-10 and IFN-γ with Allergic Phenotypes

ISRN Allergy ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-6
Author(s):  
Guicheng Zhang ◽  
Catherine M. Hayden ◽  
Jack Goldblatt ◽  
Patrick Holt ◽  
Peter N. Le Souëf
Keyword(s):  
Total Serum ◽  
Staphylococcal Enterotoxin B ◽  
Th2 Cytokines ◽  
Th2 Cytokine ◽  
Regulatory Cytokine ◽  
Cytokine Levels ◽  
Dust Mite ◽  
Th1 Cytokine ◽  
Ifn Γ ◽  
Th1 Cytokines

The expression of allergic phenotypes involves complex inter-relationships among several Th2 and Th1 cytokines as well as the regulator cytokine interleukin (IL)-10. These direct or indirect interrelationships may distort the true associations of cytokine responses with these phenotypes. In this study, we aimed to clarify the effects of the regulatory cytokine IL-10 and Th1 cytokine interferon-gamma (IFN-γ) on allergic phenotypes after adjusting for the correlations with Th2 cytokines. After adjusting for Th2 cytokines, IL-10 and IFN-γ were protective against atopy. Adjusted levels of IL-10 and IFN-γ stimulated with house-dust mite (HDM) were significantly lower in atopics than non-atopics, for IL-10 adjusting for IL-5 (P=0.002), IL-13 (P=0.012), IL-9 (P=0.016), and IL-4 (P=0.043), and for IFN-γ adjusting for IL-5 (P=0.005), IL-13 (P=0.005), and IL-9 (P=0.037). IL-10 and IFN-γ levels stimulated with phytohaemagglutinin (PHA) and staphylococcal enterotoxin B (SEB) exhibited a similar pattern. The adjusted levels of IL-10 and IFN-γ stimulated with HDM, PHA or SEB were all significantly negatively correlated with total serum IgE, except for IFN-γ stimulated with SEB. Levels of Th2 cytokines distort the associations of IL-10 and IFN-γ with allergic phenotypes. Removing the covariance with Th2 cytokines, both IL-10 and IFN-γ were protective against atopy.

Regulation of interleukin-1 receptor antagonist by Th1 and Th2 cytokines

1995 ◽  
Vol 269 (1) ◽  
pp. L92-L98 ◽  
Author(s):  
J. N. Kline ◽  
P. A. Fisher ◽  
M. M. Monick ◽  
G. W. Hunninghake
Keyword(s):  
Airway Inflammation ◽  
Interleukin 1 ◽  
Th2 Cytokines ◽  
Ifn Gamma ◽  
Th1 And Th2 Cytokines ◽  
Th1 Cytokine ◽  
Specific Antagonist ◽  
T Helper Lymphocyte ◽  
Th1 And Th2

Airway inflammation is an important aspect of asthma. Recent studies of airway inflammation in asthma have focused attention on cytokines released by T helper lymphocyte type 1 (Th1)- and Th2-like T cells. Interleukin (IL)-1 is also increased in the airways of asthmatics, and it is most likely derived from airway and alveolar macrophages. The effects of Th1 or Th2 cytokines on the release of IL-1 or its specific antagonist, IL-1ra, have not been well studied. We examined the response of THP-1 cells, a myelomonocytic cell line, to stimulation with various Th1 and Th2 cytokines and found that IL-4, IL-10, and IFN-gamma increased IL-1ra mRNA and protein release. The increase in mRNA was not due to an increase in IL-1ra mRNA stability. IL-4 (10 ng/ml) increased IL-1ra release from 9,641 +/- 322 [from cells stimulated with lipopolysaccharide (LPS) alone] to 50,796 +/- 1,917 pg/ml (from cells stimulated with LPS and IL-4). IL-10 (10 ng/ml) caused a similar upregulation of IL-1ra from LPS-stimulated cells: 87,478 +/- 7,808 compared with 8,004 +/- 1,166 pg/ml released from the cells stimulated with LPS alone. Cells stimulated with IFN-gamma (100 U/ml) and LPS released 27,854 +/- 3,626 pg/ml of IL-1ra, compared with 9,069 +/- 236 pg/ml in the presence of LPS alone. In addition, the Th1 cytokine, IFN-gamma, but not the Th2 cytokines, IL-4 and IL-10, upregulated IL-1 beta mRNA and increased the release of IL-1 beta protein. Similar studies were performed using freshly isolated monocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

The impact of a multi-epitope melanoma helper peptide vaccine on Th1 cytokine production by responding lymphocytes.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e19028-e19028
Author(s):  
Patrick Michael Dillon ◽  
Walter C. Olson ◽  
Kimberly A. Chianese-Bullock ◽  
Andrea Czarkowski ◽  
Craig L. Slingluff
Keyword(s):  
T Cells ◽  
Cytokine Production ◽  
Cytokine Profile ◽  
Helper T Cells ◽  
Th2 Cytokines ◽  
Measurable Disease ◽  
Th1 And Th2 Cytokines ◽  
Th1 Cytokine ◽  
The Impact ◽  
Th1 And Th2

e19028 Background: Melanomas produce soluble and cell-associated molecules that can suppress or alter antitumor immunity. Preclinical studies suggest the disease burden may alter the cytokine profile of helper T cell responses to cancer antigens. To describe the vaccine-induced production of Th2 or Th1 responses to helper peptides in the setting of advanced melanoma, we measured cytokine production of helper T cells responding to vaccination by 6 melanoma helper peptides (6MHP). We then analyzed results by measurable disease status. Methods: Thirty-nine patients with stage IIIB-IV melanoma received a 6MHP vaccine as a part of the UVA Mel41 clinical trial. For analysis of this correlative endpoint, antigen-reactive T cells were exposed to antigen, and supernatants (days 2 and 5) were assayed by cytokine bead arrays for Th1 and Th2 cytokines. Results: The dominant Th1 and Th2 cytokines detected were IFN-g and IL-5, respectively, though high levels of IL-2 were also produced early by sentinel lymph node lymphocytes. Th1 cytokine responses predominated both pre and post vaccine. Peripheral blood lymphocytes from patients with clinically measurable disease produced similar levels of total cytokine as patients with no evidence of disease (111pg/ml versus 174pg/ml respectively, p=0.44). For both disease statuses, the cytokine profile was Th1-dominant in most patients. Total cytokine production varied significantly among patients and varied over time but persisted up to nine months post-vaccine. Conclusions: The MHC class II-associated peptides used in this study induced helper T cells with a Th1-biased cytokine response in both PBMC and sentinel immunized nodes. However, both groups of patients can mount a Th1 dominant response to these peptides, which may persist long after the vaccination sequence. Future studies are needed to test newer vaccine adjuvants in combination with these peptides.

scholarly journals Dendritic Cell Function during Chronic Hepatitis C Virus and Human Immunodeficiency Virus Type 1 Infection

2007 ◽  
Vol 14 (9) ◽  
pp. 1127-1137 ◽  
Author(s):  
Zheng Fan ◽  
Xiao-Li Huang ◽  
Pawel Kalinski ◽  
Stephen Young ◽  
Charles R. Rinaldo
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Hepatitis C ◽  
Hcv Infection ◽  
Immunodeficiency Virus ◽  
Chronic Hcv Infection ◽  
Ifn Γ ◽  
Chronic Hcv ◽  
Hiv 1

ABSTRACT Hepatitis C virus (HCV) infection can persist despite HCV-specific T-cell immunity and can have a more aggressive course in persons coinfected with human immunodeficiency virus type 1 (HIV-1). Defects in antigen-presenting, myeloid dendritic cells (DCs) could underlie this T-cell dysfunction. Here we show that monocyte-derived DCs from persons with chronic HCV infection, with or without HIV-1 coinfection, being treated with combination antiretroviral therapy produced lower levels of interleukin 12 (IL-12) p70 in response to CD40 ligand (CD40L), whereas the expression of DC surface activation and costimulatory molecules was unimpaired. The deficiency in IL-12 production could be overcome by addition of gamma interferon (IFN-γ) with CD40L, resulting in very high, comparable levels of IL-12 production by DCs from HCV- and HIV-1-infected subjects. Smaller amounts of IL-12 p70 were produced by DCs treated with the immune modulators tumor necrosis factor alpha and IL-1β, with or without IFN-γ, and the amounts did not differ among the uninfected and infected subjects. Blocking of IL-10 with an anti-IL-10 monoclonal antibody in the CD40L-stimulated DC cultures from HCV-infected persons increased the level of IL-12 p70 production. The ability of DCs from HCV-infected persons to stimulate allogeneic CD4+ T cells or induce IL-2, IL-5, or IL-10 in a mixed lymphocyte reaction was not impaired. Thus, myeloid DCs derived from persons with chronic HCV infection or with both HCV and HIV-1 infections have defects in IL-12 p70 production related to IL-10 activity that can be overcome by treatment of the DCs with CD40L and IFN-γ. DCs from these infected subjects have a normal capacity to stimulate CD4+ T cells. The functional effectiveness of DCs derived from HCV-infected individuals provides a rationale for the DC-based immunotherapy of chronic HCV infection.

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