HLA Class I: Functionality

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The page below is a sample from the LabCE course The Human Leukocyte Antigen (HLA) System. Access the complete course and earn ASCLS P.A.C.E.-approved continuing education credits by subscribing online.

Learn more about The Human Leukocyte Antigen (HLA) System (online CE course)
HLA Class I: Functionality

HLA Class I molecules present intracellular (endogenous) antigens to CD8+ Cytotoxic T cells and/or Natural Killer Cells. Normal cellular processes involve intracellular proteases that ship intracellular peptides to the cell surface for immune system monitoring.
In normal CD8+ T cells, the Toll Like Receptor (TLR) interacts with the CD8 protein to restrict and selectively bind to HLA class I glycoproteins found on all nucleated cells to "screen" for foreign antigen. Virally-infected or cancer cells would produce non-self proteins. These non-self proteins are expressed in the binding domain of HLA class I with TLR/CD8 complex. This activates the CD8+ T cells to release cytolytic granules that trigger the bound cell to induce apoptosis (programmed cell death).
Some pathogens and diseases may dampen, or decrease, the expression of HLA class I proteins. This decreases the ability of CD8 T cells to find virally-infected or cancer cells. Fortunately, these virally-infected or cancer cells do not escape from Natural Killer [NK] cells. Lack of HLA class I expression on viral or cancer host cells prevents the inhibition of CD56+ NK cells. Loss of HLA class I in a host cell provides no inhibitory signals to the NK cell, which activates NK cells to kill the targeted cell with a targeted release of apoptotic granules.
9. Scray. "Simplified diagram of cytoplasmic protein degradation by the proteasome, transport into endoplasmic reticulum by TAP complex, loading on MHC class I, and transport to the surface for presentation." Wikimedia Commons, 16 Mar 2009, https://commons.wikimedia.org/wiki/File:MHC_Class_I_processing.svg

Simplified diagram of cytoplasmic protein degradation by the proteasome, transport into endoplasmic reticulum by TAP complex, loading on MHC class I, and transport to the surface for presentation (9).