scholarly journals Gamma Interferon-Dependent Protection of the Mouse Upper Respiratory Tract following Parenteral Immunization with a Respiratory Syncytial Virus G Protein Fragment

2002 ◽  
Vol 76 (20) ◽  
pp. 10203-10210 ◽  
Author(s):  
Helene Plotnicky-Gilquin ◽  
Dominique Cyblat-Chanal ◽  
Jean-Pierre Aubry ◽  
Thierry Champion ◽  
Alain Beck ◽  
...  
Keyword(s):  
G Protein ◽  
Cell Epitope ◽  
T Helper Cell ◽  
Helper Cell ◽  
Amino Acid Residues ◽  
Upper Respiratory Tract ◽  
T Helper ◽  
Parenteral Immunization ◽  
Ifn Γ ◽  
Syncytial Virus

ABSTRACT The protective mechanisms induced in the mouse upper respiratory tract (URT) after intraperitoneal immunization with G2Na, a recombinant respiratory syncytial virus (RSV) G protein fragment (amino acid residues 130 to 230), were investigated. This protection was recently shown to be mediated by CD4+ T cells and to be critically dependent on the cysteines and amino acids 193 and 194 (H. Plotnicky-Gilquin, A. Robert, L. Chevalet, J.-F. Haeuw, A. Beck, J.-Y. Bonnefoy, C. Brandt, C.-A. Siegrist, T. N. Nguyen, and U. F. Power, J. Virol. 74:3455-3463, 2000). On G2Na, we identified a domain (amino acid residues 182 to 198) responsible for the T-helper-cell activity. This region coincided with a peptide designed AICK (residues 184 to 198) which includes the previously identified murine and human T-helper-cell epitope on the native G protein (P. W. Tebbey, M. Hagen, and G. E. Hancock, J. Exp. Med. 188:1967-1972, 1998). Immunization with AICK, in alum or complete Freund's adjuvant, significantly reduced nasal RSV titers in normal BALB/c mice. However, although lung protection was induced, in contrast to the case with live RSV, neither AICK nor G2Na was able to prevent nasal infection in gamma interferon (IFN-γ)-knockout mice. Anti-IFN-γ neutralizing antibodies partially inhibited URT protection after administration to G2Na-immunized BALB/c mice. Furthermore, while purified CD4+ T cells from BALB/c mice immunized with G2Na or AICK significantly reduced lung and nasal infection of naive recipient mice after adoptive transfer, the cells from IFN-γ-knockout mice had no effect. Together, these results demonstrated for the first time that the T-helper-cell epitope of RSV G protein induces URT protection in mice after parenteral immunization through a Th1-type, IFN-γ-dependent mechanism.

Increased T-helper Cell 2 Response in Infants With Respiratory Syncytial Virus Bronchiolitis Hospitalized Outside Epidemic Peak

2020 ◽  
Vol 39 (1) ◽  
pp. 61-67 ◽  
Author(s):  
Raffaella Nenna ◽  
Giorgio Fedele ◽  
Antonella Frassanito ◽  
Laura Petrarca ◽  
Greta Di Mattia ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
T Helper Cell ◽  
Helper Cell ◽  
T Helper ◽  
Respiratory Syncytial Virus Bronchiolitis ◽  
Syncytial Virus

scholarly journals CD4+ T-Cell-Mediated Antiviral Protection of the Upper Respiratory Tract in BALB/c Mice following Parenteral Immunization with a Recombinant Respiratory Syncytial Virus G Protein Fragment

2000 ◽  
Vol 74 (8) ◽  
pp. 3455-3463 ◽  
Author(s):  
Hélène Plotnicky-Gilquin ◽  
Alain Robert ◽  
Laurent Chevalet ◽  
Jean-Francois Haeuw ◽  
Alain Beck ◽  
...  
Keyword(s):  
T Cells ◽  
Respiratory Syncytial Virus ◽  
G Protein ◽  
Adoptive Transfer ◽  
Critical Role ◽  
Upper Respiratory Tract ◽  
Protein Fragment ◽  
Parenteral Immunization ◽  
Upper Respiratory ◽  
Syncytial Virus

ABSTRACT We analyzed the protective mechanisms induced against respiratory syncytial virus subgroup A (RSV-A) infection in the lower and upper respiratory tracts (LRT and URT) of BALB/c mice after intraperitoneal immunization with a recombinant fusion protein incorporating residues 130 to 230 of RSV-A G protein (BBG2Na). Mother-to-offspring antibody (Ab) transfer and adoptive transfer of BBG2Na-primed B cells into SCID mice demonstrated that Abs are important for LRT protection but have no effect on URT infection. In contrast, RSV-A clearance in the URT was achieved in a dose-dependent fashion after adoptive transfer of BBG2Na-primed T cells, while it was abolished in BBG2Na-immunized mice upon in vivo depletion of CD4+, but not CD8+, T cells. Furthermore, the conserved RSV-A G protein cysteines and residues 193 and 194, overlapping the recently identified T helper cell epitope on the G protein (P. W. Tebbey et al., J. Exp. Med. 188:1967–1972, 1998), were found to be essential for URT but not LRT protection. Taken together, these results demonstrate for the first time that CD4+ T cells induced upon parenteral immunization with an RSV G protein fragment play a critical role in URT protection of normal mice against RSV infection.

Syntheses and Immunological Evaluation of Self‐Adjuvanting Clustered N ‐Acetyl and N ‐Propionyl Sialyl‐Tn Combined with a T‐helper Cell Epitope as Antitumor Vaccine Candidates

2018 ◽  
Vol 130 (27) ◽  
pp. 8351-8356 ◽  
Author(s):  
Tsung‐Che Chang ◽  
Yoshiyuki Manabe ◽  
Yukari Fujimoto ◽  
Shino Ohshima ◽  
Yoshie Kametani ◽  
...  
Keyword(s):  
Cell Epitope ◽  
T Helper Cell ◽  
Helper Cell ◽  
T Helper ◽  
Vaccine Candidates ◽  
Antitumor Vaccine ◽  
Immunological Evaluation ◽  
Sialyl Tn

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.

scholarly journals A Polypeptide of Tumor-Associated Antigen L6 with Intrinsic Adjuvant Activity Enhances Antitumor Immunity

Vaccines ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 620
Author(s):  
Yuh-Pyng Sher ◽  
Kit Man Chai ◽  
Wen-Ching Chen ◽  
Kuan-Yin Shen ◽  
I-Hua Chen ◽  
...  
Keyword(s):  
Immune Responses ◽  
Cancer Vaccine ◽  
Antitumor Immunity ◽  
Cell Epitope ◽  
Specific Treatment ◽  
T Helper Cell ◽  
Helper Cell ◽  
Peptide Vaccines ◽  
T Helper ◽  
Tumor Associated Antigen

Peptide vaccines are safe, and aim to elicit and expand tumor-specific immunity so as to eradicate tumors. However, achieving strong and long-lasting anti-tumor immunity with peptide vaccines for the antigen-specific treatment of cancer is challenging, in part because their efficacy depends on strong adjuvants or immunomodulators. We approached this problem by conjugating an epitope-based cancer vaccine with a lipidated sequence (an immunomodulator) to elicit a strong immune response. Lipidated and non-lipidated polyepitope proteins were generated that contained the universal T helper cell epitope (pan-DR), B cell epitopes, and the extended loop sequence of extracellular domain 2 of tumor-associated antigen L6 (TAL6). We show that the lipidated polyepitope cancer vaccine can activate bone marrow-derived dendritic cells, and trigger effective antigen-specific antibody and T helper cell responses, more effectively than the non-lipidated vaccine. Moreover, potent T cell immune responses were elicited in mice inoculated with the lipidated polyepitope cancer vaccine, providing protective antitumor immunity in mice bearing TAL6 tumors. Our study demonstrates that a lipidated polyepitope cancer vaccine could be employed to generate potent anti-tumor immune responses, including humoral and cellular immunity, which could be beneficial in the treatment of TAL6+ cancer.

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.

Comprehensive Intestinal T Helper Cell Profiling Reveals Specific Accumulation of IFN-γ+IL-17+Coproducing CD4+ T Cells in Active Inflammatory Bowel Disease

2014 ◽  
Vol 20 (12) ◽  
pp. 2321-2329 ◽  
Author(s):  
Anna-Maria Globig ◽  
Nadine Hennecke ◽  
Bianca Martin ◽  
Maximilian Seidl ◽  
Günther Ruf ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
Bowel Disease ◽  
Cd4 T Cells ◽  
T Helper Cell ◽  
Helper Cell ◽  
T Helper ◽  
Specific Accumulation ◽  
Inflammatory Bowel ◽  
Ifn Γ
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