Figure 1. At the cellular level, CD8 cytotoxic T cells ( ), with the help of CD4 T-helper cells, lyse HIV-infected cells. Soluble factors and neutralizing antibodies inhibit viral replication. Macrophage-tropic HIV ( ) infects cells bearing CD4 and CCR5 co-receptor. T-tropic HIV ( ) infects cells bearing CD4 and CXCR4 co-receptor. Co-receptors and their ligands (regulated on activation, normal T expressed and secreted [ ]; macrophage inflammatory protein [ ]-1α; MIP-1β; and stromal cell–derived factor [ ]-1) are discussed in part 2 of this review. At the local level, mucosal CTLs and mucosal IgA may inhibit initial viral replication. Concomitant infections activate T cells, providing target cells for HIV to infect. Systemically, such inhibiting factors as CTLs, antibodies, interferon ( ), and interleukin ( )-16 are countered with such stimulating factors as tumor necrosis factor ( ), IL-1, IL-6, and co-infections. Interleukin-10 inhibits IL-6 and TNF-α. Cytokines are discussed in part 2 of this review. The rectangular bars indicate sites of inhibition. STD = sexually transmitted disease.
Schematic overview of host responses at the cellular, local, and systemic levels.+CTLs+R5X4RANTESMIPSDFIFNILTNFGrahic Jump Location
Figure 2. An antigen-presenting cell presents an HIV epitope in association with an MHC class II molecule, which interacts with a CD4 T-helper cell whose T-cell receptor ( ) recognizes that particular epitope. The T-helper cell is then activated and stimulates the CD8 CTL. The CTL encounters an HIV epitope presented by an antigen-presenting cell in association with an MHC class I molecule. The activated CTL lyses the HIV-infected cell. IL-2 = interleukin-2.
Interactions among cytotoxic T-cell lymphocytes (CTLs), T-helper cells, and antigen-presenting cells.+TCR+Grahic Jump Location