Treatment with monoclonal antibodies (mAbs) against the 4-1BB T-cell activation molecule eradicate established tumors

1997 ◽  
Vol 56 (1-3) ◽  
pp. 362 ◽  
Author(s):  
I Melero
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation

T-Cell Activation by Bispecific Monoclonal Antibodies for Lysis of Renal Cell Carcinoma In Vitro

1992 ◽  
pp. 156-161
Author(s):  
J. van Dijk ◽  
S. Th. Zegveld ◽  
J. D. H. van Eendenburg ◽  
E. Braakman ◽  
G. J. Fleuren ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Monoclonal Antibodies ◽  
T Cell ◽  
Cell Carcinoma ◽  
T Cell Activation ◽  
Renal Cell ◽  
Cell Activation

scholarly journals Inhibition of T cell activation in vivo with mixtures of monoclonal antibodies specific for I-A and I-A/E molecules.

1981 ◽  
Vol 154 (1) ◽  
pp. 188-192 ◽  
Author(s):  
J Sprent ◽  
E A Lerner ◽  
J Bruce ◽  
F W Symington
Keyword(s):  
T Cells ◽  
Monoclonal Antibodies ◽  
T Cell ◽  
B Cells ◽  
T Cell Activation ◽  
Cell Activation ◽  
Marked Contrast ◽  
Sheep Erythrocytes

(CBA x B6)F1 (Iak x Iab) T cells were activated to sheep erythrocytes in irradiated F1 mice in the presence of various monoclonal anti-Ia reagents and then tested for their capacity to collaborate with B cells from B10.BR (I-Ak, I-Ek) (kk), B10.A(4R) (kb), and B10 (bb) mice. Anti-I-Ak antibodies blocked the generation of help for B10.A(4R) B cells, but not B10.BR or B10 B cells. An anti-I-Ab antibody blocked help for B10 B cells, but not for B10.BR or B10.A(4R) B cells. An antibody (Y-17) specific for I-Ak/Ek and I-Ab/Ek molecules, but not for I-Ak or I-Ab molecules, failed to impair the generation of help for B10.BR, B10.A (4R), or B10 B cells. In marked contrast to injecting each antibody separately, a mixture of anti-I-Ak and anti-I-Ak,b/Ek (Y-17) antibodies virtually abolished the generation of help for B10.BR B cells. A mixture of anti-I-Ak and anti-I-Ab antibodies effectively blocked help for (4R x B10)F1 B cells, i.e., cells expressing hybrid I-A molecules. These two antibodies only marginally impaired help for (CBA x B6)F1 B cells. To block help for (CBA x B6)F1 B cells required selection in the presence of a cocktail of anti-I-Ak, anti-I-Ab, and anti-I-Ak,b/Ek antibodies. The implications of these findings are discussed.

scholarly journals Advances and challenges in the treatment of myasthenia gravis

2021 ◽  
Vol 14 ◽  
pp. 175628642110654
Author(s):  
Christiane Schneider-Gold ◽  
Nils Erik Gilhus
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
Myasthenia Gravis ◽  
T Cell Activation ◽  
Cell Activation ◽  
New Drugs ◽  
Duration Of Treatment ◽  
Positive Effects ◽  
New Therapeutic Approaches ◽  
Chronic Autoimmune Disease

Myasthenia gravis (MG) is a chronic autoimmune disease with fluctuating muscle weakness and fatigability. Standard immunomodulatory treatment may fail to achieve sufficient improvement with minimal symptom expression or remission of myasthenic symptoms, despite adequate dosing and duration of treatment. Treatment-resistant MG poses a challenge for both patients and treating neurologists and requires new therapeutic approaches. The spectrum of upcoming immunotherapies that more specifically address distinct targets of the main immunological players in MG pathogenesis includes T-cell directed monoclonal antibodies that block the intracellular cascade associated with T-cell activation, monoclonal antibodies directed against key B-cell molecules, as well as monoclonal antibodies against the fragment crystallizable neonatal receptor (FcRn), cytokines and transmigration molecules, and also drugs that inhibit distinct elements of the complement system activated by the pathogenic MG antibodies. The review gives an overview on new drugs being evaluated in still ongoing or recently finished controlled clinical trials and drugs of potential benefit in MG due to their mechanisms of action and positive effects in other autoimmune disorders. Also, the challenges associated with the new therapeutic options are discussed briefly.

scholarly journals Immunotherapy in hematologic malignancies

2019 ◽  
Vol 27 (S2) ◽  
Author(s):  
R.R. Kansara ◽  
C. Speziali
Keyword(s):  
Monoclonal Antibody ◽  
Monoclonal Antibodies ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Checkpoint Inhibitors ◽  
Cytotoxic T Cells ◽  
Hematologic Malignancies ◽  
Immune Checkpoints ◽  
Hematologic Neoplasms

The management of hematologic malignancies has traditionally relied on chemotherapy regimens, many of which are still in use today. However, with advancements in the knowledge of tumour pathophysiology, therapies are continually evolving. Monoclonal antibodies against specific targets on tumour cells are now widely used to treat hematologic malignancies, either in combination with chemotherapy or as single agents. Rituximab, a monoclonal antibody against the CD20 antigen, is a good example of successful monoclonal antibody therapy that has improved outcomes for patients with B cell non-Hodgkin lymphomas. Monoclonal antibodies are now being used against the immune checkpoints that function to inhibit T cell activation and subsequent tumour eradication by those cytotoxic T cells. Such therapies enhance T cell–mediated tumour eradication and are widely successful in treating patients with solid tumours such as malignant melanoma. Now, they are slowly finding their place in the management of hematologic neoplasms. Even though, currently, immune checkpoint inhibitors are used for relapsed or refractory hematologic neoplasms, trials are ongoing to evaluate their role in frontline treatment. Our review focuses on the current use of immunotherapies in various hematologic malignancies.

Juzentaihoto Exerts Anti-Allergic Effects by Inhibiting Effector T-Cell Activation and Inducing and/or Activating Regulatory T Cells in a Murine Model of Contact Hypersensitivity

2021 ◽  
pp. 1-13
Author(s):  
Atsushi Tsuge ◽  
Sho Yonekura ◽  
Satomi Watanabe ◽  
Yuta Kurosaki ◽  
Shinsuke Hisaka ◽  
...  
Keyword(s):  
T Cells ◽  
Monoclonal Antibodies ◽  
T Cell ◽  
Regulatory T Cells ◽  
T Cell Activation ◽  
Cell Activation ◽  
Effector T Cells ◽  
Contact Hypersensitivity ◽  
Dependent Manner ◽  
Effector T Cell

<b><i>Background:</i></b> Juzentaihoto (JTT) is a Kampo prescription that has been used clinically for treating skin diseases such as atopic dermatitis in Japan. We have previously studied the anti-allergic effects of JTT on 2,4,6-trinitrochlorobenzene (TNCB)-induced contact hypersensitivity (CHS) in mice and demonstrated that it significantly suppresses ear swelling in a dose-dependent manner. However, the mechanism underlying the anti-allergic actions of JTT is obscure. <b><i>Methods:</i></b> We investigated the mechanism underlying the anti-allergic effects of JTT using a TNCB-induced murine CHS model and adoptive cell transfer experiments. <b><i>Results:</i></b> We showed that the anti-allergic effects of JTT are due to inhibition of effector T-cell activation and induction and/or activation of regulatory T cells. Furthermore, ex vivo experiments confirmed the effect of JTT on the activation of effector T cells and regulatory T cells, as interferon-γ production decreased, whereas interleukin (IL)-10 production increased, in the cultured lymphocytes obtained from 5% TNCB-sensitized mice treated with anti-CD3ε and anti-CD28 monoclonal antibodies. Flow cytometry showed that the CD4<sup>+</sup>CD25<sup>+</sup>Foxp3<sup>+</sup>, CD4<sup>+</sup>CD25<sup>+</sup>Foxp3<sup>−</sup>, and CD8<sup>+</sup>CD122<sup>+</sup> cell population increased after oral administration of JTT. Finally, the anti-allergic effect of JTT by inducing and/or activating regulatory T cells (Tregs) was confirmed to be mediated by IL-10 through in vivo neutralization experiments with anti-IL-10 monoclonal antibodies. <b><i>Conclusion:</i></b> We suggested that JTT exerts anti-allergic effects by regulating the activation of effector T cells and Tregs involved in murine CHS model.

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