CD4+ T cells tumor specific response exists in L615 leukemia mice: adoptive transfer in combination with cyclophosphamide.
نویسندگان
چکیده
AIM L615 leukemia cell line is a transplantable acute lymphocytic leukemia model with the CD4 positive phenotype. In this study, we explored whether tumor response specific T cells can be separated from the live leukemia mice or not. METHODS The mutant HGPRT- L615 cell line was first established. The splenocytes from HGPRT- L615 leukemia mice were cultured and expanded in mixed tumor-lymphocytes culture manner. The expanded T cells were sorted with FACScan. Then their killing capacity, IFN-gamma release as well as antitumor capacity in adoptive transfer experiments were analyzed. RESULTS The expanded response T cells are mostly CD4 positive. The CD4 positive T cells showed high release of IFN-gamma upon stimulation but lacked significant cytotoxicity. In immunochemotherapy model, these CD4 positive T cells can cure most leukemia mice. CONCLUSIONS We demonstrated the feasibility of separation of tumor response specific CD4+ T cells from CD4+ L615 leukemia mice. These CD4+ T cells can cure leukemia mice upon adoptive transfer in combination with cyclophosphamide pretreatment.
منابع مشابه
Reversal of CD8+ T cell ignorance and induction of anti-tumor immunity by peptide-pulsed APC.
In the present report, we have studied the potential of naive and activated effector CD8(+) T cells to function as anti-tumor T cells to a solid tumor using OVA-specific T cells from TCR-transgenic OT-I mice. Adoptive transfer of naive OT-I T cells into tumor-bearing syngeneic mice did not inhibit tumor cell growth. The adoptively transferred OT-I T cells did not proliferate in lymphoid tissue ...
متن کاملAdoptive transfer of anti-CD3-activated CD4+ T cells plus cyclophosphamide and liposome-encapsulated interleukin-2 cure murine MC-38 and 3LL tumors and establish tumor-specific immunity.
The infusion of anti-CD3-activated murine T cells plus interleukin-2 (IL-2) exerts antitumor effects against several tumors in murine immunotherapy models. This study compares the therapeutic efficacy of anti-CD3-activated CD4+ or CD8+ T-cell subsets, when given with cyclophosphamide (Cy) and liposome-encapsulated IL-2 (L-IL2) in a murine model. C57BL/6 mice bearing subcutaneous (S.C.) MC-38 co...
متن کاملUnleashing the power of anti-tumor CD4+ T cells: novel insights into the curative mechanisms of chemoimmunotherapy for cancer
Background CD4 T cells are critical mediators of anti-tumor immunity and orchestrate a broad range of immune responses against cancer. Previous studies from our lab and others have demonstrated that, adoptive transfer of tumor specific CD4 T cells to lymphopenic hosts led to eradication of established tumors in mice models. Accumulating evidence from preclinical and clinical studies also sugges...
متن کاملImmunosuppressive myeloid cells induced by chemotherapy attenuate antitumor CD4+ T-cell responses through the PD-1-PD-L1 axis.
In recent years, immune-based therapies have become an increasingly attractive treatment option for patients with cancer. Cancer immunotherapy is often used in combination with conventional chemotherapy for synergistic effects. The alkylating agent cyclophosphamide (CTX) has been included in various chemoimmunotherapy regimens because of its well-known immunostimulatory effects. Paradoxically, ...
متن کاملسطح بالای پاسخ ایمنی اختصاصی لنفوسیتهای CD4+وCD8+ نسبت به سیتومگالوویروس و همبستگی بین آنها در بیماران مبتلا به لوسمی لنفوسیتی مزمن سلولB
High level of CMV-specific CD4+ and CD8+cells Immune Response and Correlation Between them in B-cell Chronic Lymphocytic Leukemia Patients B. Pourgheysri [1] , P. Moss [2] Received: 10/09/07 Sent for Revision: 05/03/08 Received Revised Manuscript: 06/12/08 Accepted: 30/12/08 Background and Objective: Chronic lymphocytic leukemia (CLL) is characterized by a monoclonal proliferation o...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Experimental oncology
دوره 26 2 شماره
صفحات -
تاریخ انتشار 2004