scholarly journals Adoptive cell therapy with CD4+ T helper 1 cells and CD8+ cytotoxic T cells enhances complete rejection of an established tumour, leading to generation of endogenous memory responses to non-targeted tumour epitopes

2017 ◽  
Vol 6 (10) ◽  
pp. e160 ◽  
Author(s):  
Kunyu Li ◽  
Braeden Donaldson ◽  
Vivienne Young ◽  
Vernon Ward ◽  
Christopher Jackson ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Therapy ◽  
Cytotoxic T Cells ◽  
Adoptive Cell Therapy ◽  
T Helper ◽  
T Helper 1 ◽  
Complete Rejection ◽  
T Helper 1 Cells

Curcumin converts Foxp3+ regulatory T cells to T helper 1 cells in patients with lung cancer

2017 ◽  
Vol 119 (2) ◽  
pp. 1420-1428 ◽  
Author(s):  
Jian Y. Zou ◽  
Chun H. Su ◽  
Hong H. Luo ◽  
Yi Y. Lei ◽  
Bo Zeng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
T Cells ◽  
Regulatory T Cells ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 1 Cells

Regulatory T Cells Suppress Development of Colitis, Blocking Differentiation of T-Helper 17 Into Alternative T-Helper 1 Cells

2011 ◽  
Vol 141 (3) ◽  
pp. 1014-1023 ◽  
Author(s):  
Tomohisa Sujino ◽  
Takanori Kanai ◽  
Yuichi Ono ◽  
Yohei Mikami ◽  
Atsushi Hayashi ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 17 ◽  
T Helper 1 Cells

Combination of gemcitabine and adoptive cell therapy of autologous anti-tumor CTL induces clinical activities in patients with refractory lung cancer

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 3053-3053
Author(s):  
U. Toh ◽  
T. Fujii ◽  
S. Takamori ◽  
M. Fukunaga ◽  
E. Ogo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
T Cells ◽  
Cell Therapy ◽  
Tumor Cells ◽  
Cytotoxic T Cells ◽  
Adoptive Cell Therapy ◽  
Autologous Tumor ◽  
Remarkable Change ◽  
Synergistic Enhancement ◽  
Ifn Γ

3053 Background: Cytotoxic T cells selectively kill autologous tumor cells is powerful for adoptive cell therapy of cancer. Gemcitabine (GEM) is able to induce molecular changes in cancer cells that make them to induce an antigen specific CTL response. This study was to evaluate the anti-tumor and the immunological activity using the CTL in combination with GEM. Methods: The 50Gy irradiated autologous tumor cells were cocultured with PBMCs and CTLs was developed with RPMI 1640 and rIL-2 (50 u/ml) for 7–14 days. Nine pts with non small cell lung cancer failed their prior chemotherapy were enrolled this pilot study. GEM regimen [intravenous (iv.) GEM (1000mg/m2) - day 1, 8 and 15 ] was started without CTL administration for 1st cycle. GEM was administered at least 2 cycles with a 1-week interval and combined with iv. CTL therapy (0.9 x 108 - 4.6 x 108 cells/injection + IL-2 0.4 MIU; biweekly for 6 to 12 injections) from 2nd cycle. The mean total administered T cells were reached to 3.9 x 109 - 5.6 x 109. PBMCs were analyzed their surface markers by Flow Cytometry and the cytokine productions of IFN-γ etc. in the serum were measured by ELISA before and after 1st cycle of GEM administration and 3rd cycles of CTL injection. Results: After finishing 2 cycles of GEM and 3 injections of CTL, the ratio of CD4/CD8 in PBMCs increased in 7/9 pts. In contrast, CD3/CD19 decreased in 6/9 pts. The cytokine production of IFN-γ in the serum revealed an increase after treatment, the levels of TGF-β were decreased simultaneously. There was no remarkable change in the levels of NKG2D in the PBMCs and MIG, IP10 in the serum. The clinical response showed PR/SD/PD was 2/5/2. The tumor marker proteins (CEA) were also decreased significantly in 4 of 9 pts. The adverse effects were tolerable with grade <2 fever, nausea and fatigue and no bone marrow suppression was observed. Conclusions: These results suggested the synergistic enhancement of antitumor effect might be induced between CTLs and anti-cancer agent GEM. Marked clinical responses were observed in two pts after the treatment. Thus this chemo-immunotherapy will be applicable for the patients with refractory lung cancer. No significant financial relationships to disclose.

scholarly journals CD4+ T Helper 1 Cells Facilitate Regression of Murine Lyme Carditis

2001 ◽  
Vol 69 (9) ◽  
pp. 5264-5269 ◽  
Author(s):  
Linda K. Bockenstedt ◽  
Insoo Kang ◽  
Christopher Chang ◽  
David Persing ◽  
Adrian Hayday ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Mrna Levels ◽  
T Helper ◽  
T Helper 1 ◽  
Lyme Carditis ◽  
Deficient Mice ◽  
Αβ T Cells ◽  
T Helper 1 Cells

ABSTRACT Murine Lyme borreliosis, caused by infection with the spirocheteBorrelia burgdorferi, results in acute arthritis and carditis that regress as a result of B. burgdorferi-specific immune responses. B. burgdorferi-specific antibodies can attenuate arthritis in mice deficient in both B cells and T cells but have no effect on carditis. Because macrophages comprise the principal immune cell in carditis, T-cell responses that augment cell-mediated immunity may be important for carditis regression. To investigate this hypothesis, we examined the course of Lyme carditis in mice selectively deficient in B cells or αβ T cells. Our results show that carditis regresses in B-cell-deficient B10.Ak mice but not in αβ T-cell-deficient mice, independently of the mouse strain background. Despite prominent macrophage infiltrates, hearts from B. burgdorferi-infected αβ T-cell-deficient mice had less mRNA for tumor necrosis factor alpha as measured by reverse transcription-PCR compared to infected control mice. Anti-inflammatory cytokine mRNA levels were equivalent. Adoptive transfer of gamma interferon-secreting CD4+ T cells into infected αβ T-cell-deficient mice promoted carditis resolution. These results show that αβ T cells can promote resolution of murine Lyme carditis and are the first demonstration of a beneficial role for CD4+ T helper 1 cells in this disease.

Predominant T helper 1 cells in patients with idiopathic portal hypertension

2000 ◽  
Vol 15 (11) ◽  
pp. 1312-1317 ◽  
Author(s):  
Katsutoshi Tokushige ◽  
Katsumi Yamauchi ◽  
Tatsuji Komatsu ◽  
Ken Takasaki ◽  
Naoaki Hayashi
Keyword(s):  
Portal Hypertension ◽  
Idiopathic Portal Hypertension ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 1 Cells

scholarly journals OX40L–OX40 Signaling in Atopic Dermatitis

2021 ◽  
Vol 10 (12) ◽  
pp. 2578
Author(s):  
Masutaka Furue ◽  
Mihoko Furue
Keyword(s):  
T Cells ◽  
Atopic Dermatitis ◽  
Memory T Cells ◽  
Effector Memory ◽  
T Helper ◽  
T Helper 1 ◽  
Therapeutic Success ◽  
T Helper 2 ◽  
Promising Target ◽  
Antigen Presenting

OX40 is one of the co-stimulatory molecules expressed on T cells, and it is engaged by OX40L, primarily expressed on professional antigen-presenting cells such as dendritic cells. The OX40L–OX40 axis is involved in the sustained activation and expansion of effector T and effector memory T cells, but it is not active in naïve and resting memory T cells. Ligation of OX40 by OX40L accelerates both T helper 1 (Th1) and T helper 2 (Th2) effector cell differentiation. Recent therapeutic success in clinical trials highlights the importance of the OX40L–OX40 axis as a promising target for the treatment of atopic dermatitis.

scholarly journals Development of Autologous, Oligoclonal, Poorly Functioning T Lymphocytes in a Patient With Autosomal Recessive Severe Combined Immunodeficiency Caused by Defects of the Jak3 Tyrosine Kinase

Blood ◽  
1998 ◽  
Vol 91 (3) ◽  
pp. 949-955 ◽  
Author(s):  
Duilio Brugnoni ◽  
Luigi D. Notarangelo ◽  
Alessandra Sottini ◽  
Paolo Airò ◽  
Marta Pennacchio ◽  
...  
Keyword(s):  
T Cells ◽  
T Lymphocytes ◽  
Tyrosine Kinase ◽  
Cd4 T Cells ◽  
Severe Combined Immunodeficiency ◽  
Combined Immunodeficiency ◽  
T Helper ◽  
T Helper 1 ◽  
In Vitro Susceptibility ◽  
And Function

Abstract Defects of the common gamma chain subunit of the cytokine receptors (γc) or of Jak3, a tyrosine kinase required for γc signal transduction, result in T−B+ severe combined immunodeficiency (SCID). However, atypical cases, characterized by progressive development of T lymphocytes, have been also reported. We describe a child with SCID caused by Jak3 gene defects, which strongly but not completely affect Jak3 protein expression and function, who developed a substantial number (>3,000/μL) of autologous CD3+CD4+ T cells. These cells showed a primed/activated phenotype (CD45R0+ Fas+HLA-DR+ CD62Llo), defective secretion of T-helper 1 and T-helper 2 cytokines, reduced proliferation to mitogens, and a high in vitro susceptibility to spontaneous (caused by downregulation of bcl-2 expression) as well as activation-induced cell death. A restricted T-cell receptor repertoire was observed, with oligoclonal expansion within each of the dominant segments. These features resemble those observed in γc-/y and in Jak3−/−mice, in which a population of activated, anergic T cells (predominantly CD4+) also develops with age. These results suggest that residual Jak3 expression and function or other Jak3-independent signals may also permit the generation of CD4+ T cells that undergo in vivo clonal expansion in humans; however, these mechanisms do not allow development of CD8+ T cells, nor do they fully restore the functional properties of CD4+ T lymphocytes.

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