Mechanisms of immune effector dysfunction in myeloma. The myeloma microenvironment in posttransplant relapses is characterized by the presence of TIGIT-expressing dysfunctional T cells displaying attributes of exhaustion (shaded red) as well as interleukin-10 (IL-10)–secreting immature dendritic cells (DCs) and macrophages. T-cell exhaustion can be reversed through blockade of the immune checkpoint TIGIT. The costimulatory counterpart CD226 is expressed by nonexhausted T effectors (shaded green). BMT, bone marrow transplantation; MM, multiple myeloma. Professional illustration by Somersault18:24.

Mechanisms of immune effector dysfunction in myeloma. The myeloma microenvironment in posttransplant relapses is characterized by the presence of TIGIT-expressing dysfunctional T cells displaying attributes of exhaustion (shaded red) as well as interleukin-10 (IL-10)–secreting immature dendritic cells (DCs) and macrophages. T-cell exhaustion can be reversed through blockade of the immune checkpoint TIGIT. The costimulatory counterpart CD226 is expressed by nonexhausted T effectors (shaded green). BMT, bone marrow transplantation; MM, multiple myeloma. Professional illustration by Somersault18:24.

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