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NKG2D and Its Ligands: "One for All, All for One"
#MMPMID29662484
Zingoni A
; Molfetta R
; Fionda C
; Soriani A
; Paolini R
; Cippitelli M
; Cerboni C
; Santoni A
Front Immunol
2018[]; 9
(?): 476
PMID29662484
show ga
The activating receptor NKG2D is peculiar in its capability to bind to numerous
and highly diversified MHC class I-like self-molecules. These ligands are poorly
expressed on normal cells but can be induced on damaged, transformed or infected
cells, with the final NKG2D ligand expression resulting from multiple levels of
regulation. Although redundant molecular mechanisms can converge in the
regulation of all NKG2D ligands, different stimuli can induce specific cellular
responses, leading to the expression of one or few ligands. A large body of
evidence demonstrates that NK cell activation can be triggered by different NKG2D
ligands, often expressed on the same cell, suggesting a functional redundancy of
these molecules. However, since a number of evasion mechanisms can reduce
membrane expression of these molecules both on virus-infected and tumor cells,
the co-expression of different ligands and/or the presence of allelic forms of
the same ligand guarantee NKG2D activation in various stressful conditions and
cell contexts. Noteworthy, NKG2D ligands can differ in their ability to
down-modulate NKG2D membrane expression in human NK cells supporting the idea
that NKG2D transduces different signals upon binding various ligands. Moreover,
whether proteolytically shed and exosome-associated soluble NKG2D ligands share
with their membrane-bound counterparts the same ability to induce NKG2D-mediated
signaling is still a matter of debate. Here, we will review recent studies on the
NKG2D/NKG2D ligand biology to summarize and discuss the redundancy and/or
diversity in ligand expression, regulation, and receptor specificity.
|Animals
[MESH]
|Cytotoxicity, Immunologic
[MESH]
|Histocompatibility Antigens Class I/*metabolism
[MESH]
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