Blood Cells - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 149

Table 3.38. Examples of plasmalemmal receptors of NK cells (Source: [ 276 ]; CEACAM1:
carcinoembryonic antigen-related cell adhesion molecule-1, a.k.a. biliary glycoprotein BGP1 and
CD66a; DAP: DNAX-activation protein; DNAM: DNAX accessory molecule; KIR: killer-cell
immunoglobulin-like receptor; KLR: killer-cell lectin-like receptor; LAIR1: leukocyte-associated
immunoglobulin-like receptor-1, or CD305; NCR: natural cytotoxicity-triggering receptor; NKG2:
NK-receptor group-2 member; SLAMF: signaling lymphocytic activation molecule family mem-
ber; TIGIT: T-cell immunoreceptor with Ig and ITIM domains that binds CD155 [a.k.a. PVR
(poliovirus receptor) and nectin-like protein NecL5] and CD112 [a.k.a. PVRL2 (poliovirus
receptor-related-2), herpesvirus entry mediator-B (HVEb), and nectin-2]). These receptors can
be categorized into stimulatory (here given with corresponding adaptor molecules), inhibitory,
cytokine, chemotactic, and adhesion receptors. In addition to MHC class-1-specific receptors, other
NK cell inhibitory receptors specific for non-MHC ligands also regulate NK-cell reactivity. Agent
CD16 is the low-affinity IgG Fc receptor-3.

Receptor Members

category (adaptors)

Stimulatory NCR1/3 (CD3 ζ ,Fc γ R), NCR2 (DAP12), KLRf1,

CD16 (CD3 R), KIRs (DAP12),

NKG2c (DAP12), NKG2d (DAP10),
SLAMF3 (SAP), SLAMF4 (SAP, EAT2, ERT),
SLAMF5 (SAP, EAT2), SLAMF6 (SAP),
SLAMF7 (SAP, EAT2)

ζ ,Fc γ

Inhibitory KIRl, LIRb1, NKG2a (KLRc1), KLRg1, TIGIT,

CEACAM1, LAIR1

Cytokine IL1R, IL2R, IL12R, IL15R, IL18R, IL21R

Ifn α R

Chemotactic CCR2/5/7, CXCR1/3/4/6, CX3CR1,

S1P 5

Adhesion CD2, DNAM1, β 1 / 2 -integrins

Natural killer cell synthesizes a set of activatory and inhibitory receptors to
ensure: (1) an efficient struggle against viral infection and tumor development as
well as (2) self tolerance (Table 3.38 ). It adapts to its environment. It thus has
attributes of both innate and adaptive immunity. NK cells sense the density of
various types of plasmalemmal molecules at the surface of interacting cells. The
integration of these signals dictates the quality and intensity of the NK-cell response.
Natural killer cells release cytotoxic enzymes and cytokines to recruit other
effector immunocytes. These cytolytic effectors kill virus-infected and mutant cells
by antibody-dependent cellular cytotoxicity via granule exocytosis and subsequent
release of perforin and granzymes, in the absence of specific immunization.
They secrete immunoregulatory growth factors and cytokines (interferon- γ ,TNF α ,

TGF , gCSF [CSF3], gmCSF [CSF2], TNFSF2, and interleukins IL1 to IL3, IL5,

IL10, and IL13) and chemokines (CC-chemokine ligands CCL2 to CCL5, CXC-
chemokine ligand CXCL8 (or IL8), and XCL1) that, in particular, influence the
differentiation of cells of adaptive immunity [ 276 ].
They colocalize with other hematopoietic cells such as dendritic cells in in-
flammation sites. They also interact with macrophages and neutrophils. Conversely,

β