摘要:
Described herein are methods for treating and preventing alloantibody driven chronic graft versus host disease (cGVHD). The methods include administering to an individual in need thereof ibrutinib for treating and preventing alloantibody driven graft versus host disease.
摘要:
Methods for inhibiting antigen-specific T cell responses by use of an agent which inhibits a costimulatory signal in T cells are disclosed. Preferably, both a first agent which inhibits a costimulatory signal in the T cell (e.g., a CTLA4Ig fusion protein) and a second agent which inhibits another T cell function, such as adhesion of the T cell to a cell presenting antigen to the T cell, are used to inhibit antigen-specific T cell responses. For example, to inhibit adhesion of a T cell to a cell presenting antigen, an anti-LFA-1 antibody can be used in conjunction with a CTLA4Ig fusion protein. Alternatively, another agent which inhibits a costimulatory signal in T cells, such as an anti-B7-1 antibody or an anti-B7-2 antibody can be used with a second agent which inhibits a proliferative signal in the T cell e.g., an anti-IL-2 receptor antibody. The methods of the invention are particularly useful for inhibiting graft versus host disease and for inhibiting rejection of a transplanted tissue or organ.
摘要:
Methods for inducing T-cell non-responsiveness to donor T-cells comprised in transplantation tissues are provided. The methods involve ex vivo treatment of donor T-cells with gp39 antagonists.
摘要:
This disclosure describes methods that generally include administering to an immune compromised subject an amount of a lymphotoxin β receptor (LTβR) agonist effective to increase immune function in the subject compared to a suitable control immune compromised subject. In some cases, the method can result decreasing the period of immune deficiency in the subject compared to a suitable control immune compromised subject.
摘要:
Methods for inducing T-cell non-responsiveness to donor T-cells comprised in transplantation tissues are provided. The methods involve ex vivo treatment of donor T-cells with gp39 antagonists.