Regulatory T cells (Treg) suppress overactive immune responses by inhibiting the function of activated T cells. These cells are very important for immunological tolerance to self antigens, food, etc.
Recently, it has been reported that tumors elude the immune system via this immunosuppressive function of Treg. Therefore, a method of increasing antitumor activity by suppressing or eliminating Treg is required.
MBL sells functional analysis grade antibodies which suppress tumor growth in tumor-bearing mice. We have a wide range of antibodies against Treg marker molecules such as transcriptional factor Foxp3.
Clone DTA-1 : Functional antibody with antitumor effect
Rat Anti-Mouse GITR monoclonal antibody (Clone: DTA-1) is developed by Prof. Sakaguchi Shimon (Institute for Frontier Medical Sciences, Kyoto Univ./ Current affiliation: Osaka Univ.) and colleagues.
GITR is expressed on cell surface of Treg and activated T cells. Administration of the antibody (clone DTA-1) produced organ-specific autoimmune disease in normal mice. A single administration of DTA-1 to tumor-bearing mice provoked potent tumor-specific immunity and eradicated established tumors without eliciting overt autoimmune disease. This antibody delivers an agonistic signal that eliminates suppression by regulatory T cells without causing depletion in vivo, which may lead to the organ-specific autoimmune response and anti-tumor effect.
Clone TH6 : Functional antibody which suppresses tumor with one shot
Rat Anti-Mouse FR4 (Folate receptor 4) monoclonal antibody (Clone: TH6) is also developed by Prof. Sakaguchi Shimon and colleagues.
Single intravenous administration of this antibody significantly reduces the cell number of Treg cells in both lymph node and peripheral blood, and causes tumor rejection. FR4 is highly expressed in natural Treg cells and CD4+CD25+ T cells which infiltrate to tumor tissue. Hence, administration of TH6 causes the reduced number of Treg cells protecting the tumor from the immune system, which may result in the tumor suppression.