Figure 26. Schematic representation of the various mechanisms that the tumor microenvironment uses in suppressing the antigen-presenting capacity and function of resident DCs. Following tumor production of chemokines (e.g., CCL22), nTreg cells are expressing CCR4 and are recruited from the vascular compartment (1). Following their release from the tumor, TAAs are normally taken up by DCs (2) leading to the activation of CD4+CD25- T effector cells. The subsequent release of the immunoregulatory cytokines IL-10 and TGF-β from the tumor suppresses DC differentiation and function, resulting in a dysfunctional DC (3). The nTregs recruited by the tumor are stimulated by the dysfunctional DCs to expand (4) leading to immunosuppressive activity in the tumor environment. The TGF-b released from the tumor cells can also lead to the conversion of the CD4+CD25- T effector cells into CD4+CD25+ Treg cells, leading to further immunosuppressive activity (5). The tumor production of VEGF stimulates angiogenesis (6).

LEARN IMMUNOLOGY, GET SUMMARIES OF THE LATEST RESEARCH, EARN CPD POINTS & MORE.

See the South African Government Resource: sacoronavirus.co.za

BREAKING NEWS

PASSING OF AN IMMUNOLOGIST

CASE STUDY

Breaking News