Figure 4.

There is significant evidence that patients with severe sepsis have defective adaptive immunity. Macrophages (or monocytes) may lose expression of the Class II MHC proteins which display foreign peptide to the TCR. However, more importantly, T-cells upregulate expression of CTLA-4, an alternative ligand for the co-stimulator B7 on the antigen-presenting cell. Instead of providing co-stimulation and activation of the T-cell, which would occur if B7 interacted with CD28, interaction with CTLA-4 results in T-cell unresponsiveness and, eventually, death by apoptosis.