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.

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 The Increasing Prevalence of Crohn’s Disease in Industrialized Societies: The Price of Progress?

2005 ◽  
Vol 19 (2) ◽  
pp. 89-95 ◽  
Author(s):  
Ron W Wells ◽  
Michael G Blennerhassett
Keyword(s):  
Immune Response ◽  
Crohn’S Disease ◽  
Immune System ◽  
Crohn's Disease ◽  
T Helper Cell ◽  
Helper Cell ◽  
Cell Type ◽  
T Helper ◽  
Th2 Immune Response ◽  
Helper Cell Type

Crohn’s disease (CD) is an idiopathic inflammatory condition of the gastrointestinal system. While inflammation can activate one of a number of specific branches of the immune system, CD promotes a T helper cell type 1 (Th1) profile. The prospect that CD is a form of Th1-dominant autoimmune disease is gaining acceptance, with support from the current use of immunosuppressants. Recently, convincing evidence that the various branches of the immune system have the ability to keep each other in check has suggested that the Th1 profile of CD may stem from a greatly reduced T helper cell type 2 (Th2) immune response. A strong Th2 immune response is a characteristic of the once prevalent enteric parasitic diseases, now nearly eradicated from industrial society. This has led to the acceptance of a hygiene hypothesis, which suggests that the inverse relationship between CD and the level of a society’s industrialization is, in fact, causal -- that the lack of parasitic infections causes a weakened systemic Th2 cytokine profile, leading to elevated Th1 cytokines and, ultimately, the development of spontaneous Th1-mediated diseases such as CD. Supporting this, it has been recently demonstrated that an experimentally-induced Th2 response can help moderate Th1-dominant events in both animal and human studies. Based on this recent and convincing work, the present review focuses on the role of immunoregulation in the development of CD, with particular emphasis on the potential use of Th2-promoting agents (such as helminths or cytokines) as therapeutics in the treatment or prevention of CD.

scholarly journals Oral Tolerance: A New Tool for the Treatment of Gastrointestinal Inflammatory Disorders and Liver-Directed Gene Therapy

1999 ◽  
Vol 13 (10) ◽  
pp. 829-835 ◽  
Author(s):  
Yaron Ilan
Keyword(s):  
Gene Therapy ◽  
Immune Response ◽  
Oral Tolerance ◽  
Tolerance Induction ◽  
T Helper Cell ◽  
Helper Cell ◽  
Cell Type ◽  
T Helper ◽  
Helper Cell Type

Oral tolerance is a method of downregulating an immune response by feeding antigens. The use of oral tolerance toward adenoviruses and colitis-extracted proteins for long term gene therapy and alleviation of experimental colitis, and the mechanisms of tolerance induction are presented. Adenoviruses are efficient vectors in liver-directed gene therapy; however, the antiviral immune response precludes the ability to achieve long term gene expression and prohibits the ability to reinject the recombinant virus. Oral tolerance induction via feeding of viral-extracted proteins prevented the antiadenoviral humoral and cellular immune responses, thus enabling long term gene therapy using these viruses. Moreover, pre-existing immune response to the virus was overcome by tolerance induction, enabling prolonged gene expression in a presensitized host. Inflammatory bowel diseases are immune-mediated disorders where an imbalance between proinflammatory (T helper cell type 1) and anti-inflammatory (T helper cell type 2) cytokines are thought to play a role in the pathogenesis. In the experimental colitis model, the feeding of colitis-extracted proteins downregulated the anticolon immune response. Tolerance induction toward colitis-extracted proteins ameliorated colonic inflammation as shown by decreased diarrhea and reduction of colonic ulcerations, intestinal and peritoneal adhesions, wall thickness and edema. Histological parameters for colitis were markedly improved in tolerized animals. In both models, tolerized animals developed an increase in transforming growth factor-beta, interleukin-4 and interleukin-10, and a decrease in the mRNA of interferon-gamma lymphocytes and serum levels. Adoptive transfer of tolerized lymphocytes enabled the transfer of tolerance toward adenoviruses and colon-extracted proteins. Thus, oral tolerance induces suppressor lymphocytes that mediate immune response downregulation by induction of a shift from a proinflammatory T helper cell type 1 to an anti-inflammatory T helper cell type 2 immune response.

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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