scholarly journals Stroke-induced Immunodeficiency Promotes Spontaneous Bacterial Infections and Is Mediated by Sympathetic Activation Reversal by Poststroke T Helper Cell Type 1–like Immunostimulation

2003 ◽  
Vol 198 (5) ◽  
pp. 725-736 ◽  
Author(s):  
Konstantin Prass ◽  
Christian Meisel ◽  
Conny Höflich ◽  
Johann Braun ◽  
Elke Halle ◽  
...  
Keyword(s):  
Bacterial Infections ◽  
Focal Cerebral Ischemia ◽  
Lymphocyte Activation ◽  
T Helper Cell ◽  
Helper Cell ◽  
T Helper ◽  
Th2 Cytokine ◽  
Key Factor ◽  
Helper Cell Type ◽  
Ifn Γ

Infections are a leading cause of death in stroke patients. In a mouse model of focal cerebral ischemia, we tested the hypothesis that a stroke-induced immunodeficiency increases the susceptibility to bacterial infections. 3 d after ischemia, all animals developed spontaneous septicemia and pneumonia. Stroke induced an extensive apoptotic loss of lymphocytes and a shift from T helper cell (Th)1 to Th2 cytokine production. Adoptive transfer of T and natural killer cells from wild-type mice, but not from interferon (IFN)-γ–deficient mice, or administration of IFN-γ at day 1 after stroke greatly decreased the bacterial burden. Importantly, the defective IFN-γ response and the occurrence of bacterial infections were prevented by blocking the sympathetic nervous system but not the hypothalamo-pituitary-adrenal axis. Furthermore, administration of the β-adrenoreceptor blocker propranolol drastically reduced mortality after stroke. These data suggest that a catecholamine-mediated defect in early lymphocyte activation is the key factor in the impaired antibacterial immune response after stroke.

scholarly journals Interferon γ Stabilizes the T Helper Cell Type 1 Phenotype

2001 ◽  
Vol 194 (2) ◽  
pp. 165-172 ◽  
Author(s):  
Yongkang Zhang ◽  
Ron Apilado ◽  
John Coleman ◽  
Shlomo Ben-Sasson ◽  
Sharon Tsang ◽  
...  
Keyword(s):  
Critical Role ◽  
Interferon Γ ◽  
T Helper Cell ◽  
Helper Cell ◽  
Wild Type ◽  
T Helper ◽  
Helper Cell Type ◽  
Ifn Γ ◽  
Th 1

T helper cell (Th)1-primed CD4 T cells from wild-type donors make little interleukin (IL)-4 when restimulated under Th2 conditions. However, such restimulation of Th1-primed cells from interferon (IFN)-γ2/− or IFN-γ receptor (IFN-γR)−/− mice resulted in substantial production of IL-4 and other Th2 cytokines. Adding IFN-γ to the priming culture markedly diminished the capacity of Th1-primed IFN-γ2/− cells to express IL-4. Even IFN-γ–producing cells from IFN-γR−/− mice could acquire IL-4–producing capacity. Thus, IFN-γ is not required for the development of IFN-γ–producing capacity, but it plays a critical role in suppressing the IL-4–producing potential of Th1 cells.

The T-Helper Cell Type 1 Immune Response to Gram-Negative Bacterial Infections Is Impaired in COPD

2011 ◽  
Vol 183 (2) ◽  
pp. 204-214 ◽  
Author(s):  
Jürgen Knobloch ◽  
Katharina Schild ◽  
David Jungck ◽  
Katja Urban ◽  
Katja Müller ◽  
...  
Keyword(s):  
Immune Response ◽  
Bacterial Infections ◽  
T Helper Cell ◽  
Helper Cell ◽  
Cell Type ◽  
T Helper ◽  
Gram Negative ◽  
Helper Cell Type

scholarly journals Immunomodulation of Helicobacter Infection

1999 ◽  
Vol 13 (3) ◽  
pp. 237-241 ◽  
Author(s):  
Ken Croitoru
Keyword(s):  
Immune Response ◽  
Bacterial Infections ◽  
T Cell Response ◽  
T Helper Cell ◽  
Helper Cell ◽  
General Tendency ◽  
Cell Type ◽  
T Helper ◽  
Helper Cell Type ◽  
H Pylori

Helicobacter pylorileads to a chronic infection in humans that is associated with gastric inflammation and a vigorous immune response. Despite the humoral and cellular responses that can be detected in both human and animal models of helicobacter infection, the immune response fails to eliminate the organism. Eradication failure may be due to the niche in whichH pyloriconfines itself, well away from direct contact with elements of the immune system. Alternatively, the general tendency of the intestinal immune response to down- regulate reactivity to noninvasive luminal bacteria also may contribute to the failure to eliminatehelicobacterinfection. Results of vaccine studies in mouse models indicate that modulating the helper T cell response from a T helper cell type 1 to a T helper cell type 2 response likely is required for the prevention and elimination of helicobacter infection. Understanding the mechanisms by which the immune response controls bacterial infections will allow for the design of novel strategies of immune modulation and the development of vaccines for both the treatment and prevention ofH pylori.

scholarly journals T Helper Cell Type 2 Responsiveness Predicts Future Susceptibility to Gastrointestinal Nematodes in Humans

2004 ◽  
Vol 190 (10) ◽  
pp. 1804-1811 ◽  
Author(s):  
Joseph A. Jackson ◽  
Joseph D. Turner ◽  
Lawrence Rentoul ◽  
Helen Faulkner ◽  
Jerzy M. Behnke ◽  
...  
Keyword(s):  
Gastrointestinal Nematodes ◽  
T Helper Cell ◽  
Helper Cell ◽  
Cell Type ◽  
T Helper ◽  
Helper Cell Type

scholarly journals T helper cell type 1 (Th1), Th2 and Th17 responses to myelin basic protein and disease activity in multiple sclerosis

Immunology ◽  
2008 ◽  
Vol 125 (2) ◽  
pp. 161-169 ◽  
Author(s):  
Chris J. Hedegaard ◽  
Martin Krakauer ◽  
Klaus Bendtzen ◽  
Henrik Lund ◽  
Finn Sellebjerg ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Disease Activity ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
T Helper Cell ◽  
Helper Cell ◽  
Cell Type ◽  
T Helper ◽  
Helper Cell Type

scholarly journals Anti–Interleukin 10 Receptor Monoclonal Antibody Is an Adjuvant for T Helper Cell Type 1 Responses to Soluble Antigen Only in the Presence of Lipopolysaccharide

2000 ◽  
Vol 192 (10) ◽  
pp. 1529-1534 ◽  
Author(s):  
Antonio G. Castro ◽  
Margaret Neighbors ◽  
Stephen D. Hurst ◽  
Francesca Zonin ◽  
Regina A. Silva ◽  
...  
Keyword(s):  
T Cells ◽  
T Helper Cell ◽  
Helper Cell ◽  
Transfer Model ◽  
Soluble Antigen ◽  
Cell Type ◽  
T Helper ◽  
Peptide Antigen ◽  
Helper Cell Type

Soluble foreign antigen usually leads to a transient clonal expansion of antigen-specific T cells followed by the deletion and/or functional inactivation of the cells. As interleukin (IL)-10 is a key immunoregulatory cytokine, we questioned whether neutralization of IL-10 during priming with soluble antigen could prime for a subsequent T helper cell type 1 (Th1) effector recall response. By using an adoptive transfer model to track the fate of antigen-specific T cell receptor (TCR)-transgenic CD4+ T cells, we show that administration of soluble ovalbumin (OVA) protein, but not OVA323–339 peptide antigen, together with an anti–IL-10 receptor (R) mAb led to the enhancement of a Th1 response upon rechallenge. Lipopolysaccharide (LPS) present in the protein was necessary for priming for Th1 recall responses in the presence of anti–IL-10R mAb, as removal of LPS abrogated this effect. Moreover, addition of LPS to the peptide did not itself allow priming for recall Th1 effector responses unless endogenous levels of IL-10 were neutralized with an anti–IL-10R mAb. A significant increase in OVA-specific IgG1 and IgG2a isotypes was observed when the protein antigen was administered with anti–IL-10R mAb; however, this was not the case with peptide antigen administered together with anti–IL-10R and LPS. Our data, showing that LPS receptor signaling and neutralization of endogenous immunosuppressive cytokines is essential for Th1 priming, has important implications for the design of relevant vaccines for effective in vivo immunotherapy.

scholarly journals Crucial Role of the Interleukin 1 Receptor Family Member T1/St2 in T Helper Cell Type 2–Mediated Lung Mucosal Immune Responses

1999 ◽  
Vol 190 (7) ◽  
pp. 895-902 ◽  
Author(s):  
Anthony J. Coyle ◽  
Clare Lloyd ◽  
Jane Tian ◽  
Trang Nguyen ◽  
Christina Erikkson ◽  
...  
Keyword(s):  
Immune Responses ◽  
T Helper Cell ◽  
Helper Cell ◽  
Eosinophil Infiltration ◽  
Cell Type ◽  
T Helper ◽  
Helper Cell Type ◽  
Mucosal Immune Responses

T1/ST2 is an orphan receptor of unknown function that is expressed on the surface of murine T helper cell type 2 (Th2), but not Th1 effector cells. In vitro blockade of T1/ST2 signaling with an immunoglobulin (Ig) fusion protein suppresses both differentiation to and activation of Th2, but not Th1 effector populations. In a nascent Th2-dominated response, anti-T1/ST2 monoclonal antibody (mAb) inhibited eosinophil infiltration, interleukin 5 secretion, and IgE production. To determine if these effects were mediated by a direct effect on Th2 cells, we next used a murine adoptive transfer model of Th1- and Th2-mediated lung mucosal immune responses. Administration of either T1/ST2 mAb or T1/ST2-Ig abrogated Th2 cytokine production in vivo and the induction of an eosinophilic inflammatory response, but failed to modify Th1-mediated inflammation. Taken together, our data demonstrate an important role of T1/ST2 in Th2-mediated inflammatory responses and suggest that T1/ST2 may prove to be a novel target for the selective suppression of Th2 immune responses.

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