Exhaustion of B-cell in HIV infection


HIV-associated B-cell exhaustion was first identified in 2008, shortly after the presentation of recurrent virus-induced T-cell exhaustion, and the discovery of a subset of B cells in tonsil tissues with immune-regulatory features close to those found in T-cell exhaustions.

HIV infection immunopathogenesis entails disruptions of both innate and adaptive immunity including B cells and the antibodies they produce. Persistent HIV replication is often associated with other B-cell disruptions including over-representation of active and depleted B-cell memory subsets, the latter being the most prevalent characteristic during the chronic infection period.

In addition to the presence of additional memory B-cell subsets, which are either entirely absent or minimally present in healthy individuals' blood, HIV infection is associated with changes in the 'healthy' memory B-cell pocket. Resting memory cells B and those expressing IgM in particular, are destroyed in HIV infection.

One of T-cell exhaustion's hallmarks is that it describes a state of unresponsiveness for T cells that is unique to the recurrent pathogen. The ability to readily recognize these cells using tetramers that bind the T-cell receptor and/or test their effector activity in response to stimulation with the antigen has facilitated analyses of antigen-specific T cells.

There is several infectious and non-infectious disease settings that induce chronic or periodic activation of the immune system and lead to the over-representation of B cells with features similar to those described for tissue-like memory B cells in chronic HIV infection.

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