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(A)
(B)
(C)
328
FIGURE 15.1
Role of NK cells in parental bone marrow hybrid resistance of B6×BALB/c F1 mice. The lack of H-2 recognition by NK cells that express inhibitory receptors for
self-MHC class I molecules is involved in allogeneic bone marrow (BM) rejection. In parental (A) B6 or (B) BALB/c mice, allogeneic BM rejection is mediated by Ly49C/I
+
and Ly49G2
+
NK cells, respectively. (C) In F1 (B6×BALB/c) mice, NK cells expressing inhibitory receptors to one of the parental MHCs are capable of rejecting the bone
marrow cells (BMC) of the other parental haplotype.
blood. They are derived from CD34
+
progenitor cells in the BM and their
maturation is dependent on cytokines and stimuli that occur at distinct
stages in the BM lymphoid tissue, and peripheral blood. IL-15 is essential
for NK cell development and homeostasis, as IL-15 knockout mice lack
NK cells. Furthermore, IL-15 activity is enhanced when
trans
-presented
by other cells such as dendritic cells
[4]
. NK cells circulating in the blood
can be divided into two functionally distinct groups on the basis of cell
surface density of CD56: CD56
bright
and CD56
dim
NK cells. Comprising
about 10% of circulating NK cells, CD56
bright
NK cells are more prolifera-
tive, have a higher capacity for cytokine production following stimulation
with IL-12 and IL-18, and are poor mediators of NK cell cytotoxicity at
rest. CD56
dim
NK cells, however, are potently cytotoxic, mediate antibody-
dependent cellular cytotoxicity (ADCC) through the Fc receptor CD16, and
produce cytokines following stimulation with target cells. NK cells produce
a wide variety of cytokines and chemokines, including but not limited to,
interferon-γ (IFN-γ), granulocyte colony-stimulating factor (G-CSF), tumor
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