Marginal zone B cells are required for optimal humoral responses to allograft.

Antibody-mediated rejection (AMR) is among the leading causes of graft failure in solid organ transplantation. However, AMR treatment options are limited by an incomplete understanding of the mechanisms underlying de novo donor-specific antibody (DSA) generation. The development of pathogenic isotype-switched DSA in response to transplanted allografts is typically attributed to follicular B cells undergoing germinal center reaction whereas the contribution of other B cell subsets has not been previously addressed.

Recognizing Complexity of CD8 T Cells in Transplantation.

The major role of CD8 + T cells in clinical and experimental transplantation is well documented and acknowledged. Nevertheless, the precise impact of CD8 + T cells on graft tissue injury is not completely understood, thus impeding the development of specific treatment strategies. The goal of this overview is to consider the biology and functions of CD8 + T cells in the context of experimental and clinical allotransplantation, with special emphasis on how this cell subset is affected by currently available and emerging therapies.

p40 homodimers bridge ischemic tissue inflammation and heterologous alloimmunity in mice via IL-15 transpresentation.

Virus-induced memory T cells often express functional cross-reactivity, or heterologous immunity, to other viruses and to allogeneic MHC molecules that is an important component of pathogenic responses to allogeneic transplants. During immune responses, antigen-reactive naive and central memory T cells proliferate in secondary lymphoid organs to achieve sufficient cell numbers to effectively respond, whereas effector memory T cell proliferation occurs directly within the peripheral inflammatory microenvironment. Mechanisms driving heterologous memory T cell proliferation and effector function expression within peripheral tissues remain poorly understood.