Abstract
Natural killer (NK) cells express inhibitory receptors with varied binding affinities to specific major histocompatibility complex class I (MHC-I) haplotypes. NK cells can be classified as licensed or unlicensed based on their ability or inability to bind MHC-I, respectively. The role of donor vs host MHC on their development after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is not known. Following reciprocal MHC-disparate allogeneic transplants and during de novo NK-cell recovery, depletion of the licensed and not unlicensed population of NK cells as determined by the licensing patterns of donor MHC-I haplotypes, resulted in significantly increased susceptibility to murine cytomegalovirus (MCMV) infection. A corresponding expansion of the licensed Ly49H(+) NK cells occurred with greater interferon γ production by these cells than unlicensed NK cells in the context of donor MHC-I. Thus, NK licensing behavior to MCMV corresponds to the donor, and not recipient, MHC haplotype after allo-HSCT in mice.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1518-1521 |
| Number of pages | 4 |
| Journal | Blood |
| Volume | 122 |
| Issue number | 8 |
| DOIs | |
| State | Published - Aug 22 2013 |
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ASJC Scopus subject areas
- Hematology
- Biochemistry
- Cell Biology
- Immunology
Cite this
Murine NK-cell licensing is reflective of donor MHC-I following allogeneic hematopoietic stem cell transplantation in murine cytomegalovirus responses. / Sungur, Can M.; Tang-Feldman, Yajarayma J.; Zamora, Anthony E.; Alvarez, Maite; Pomeroy, Claire; Murphy, William J.
In: Blood, Vol. 122, No. 8, 22.08.2013, p. 1518-1521.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Murine NK-cell licensing is reflective of donor MHC-I following allogeneic hematopoietic stem cell transplantation in murine cytomegalovirus responses.
AU - Sungur, Can M.
AU - Tang-Feldman, Yajarayma J.
AU - Zamora, Anthony E.
AU - Alvarez, Maite
AU - Pomeroy, Claire
AU - Murphy, William J
PY - 2013/8/22
Y1 - 2013/8/22
N2 - Natural killer (NK) cells express inhibitory receptors with varied binding affinities to specific major histocompatibility complex class I (MHC-I) haplotypes. NK cells can be classified as licensed or unlicensed based on their ability or inability to bind MHC-I, respectively. The role of donor vs host MHC on their development after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is not known. Following reciprocal MHC-disparate allogeneic transplants and during de novo NK-cell recovery, depletion of the licensed and not unlicensed population of NK cells as determined by the licensing patterns of donor MHC-I haplotypes, resulted in significantly increased susceptibility to murine cytomegalovirus (MCMV) infection. A corresponding expansion of the licensed Ly49H(+) NK cells occurred with greater interferon γ production by these cells than unlicensed NK cells in the context of donor MHC-I. Thus, NK licensing behavior to MCMV corresponds to the donor, and not recipient, MHC haplotype after allo-HSCT in mice.
AB - Natural killer (NK) cells express inhibitory receptors with varied binding affinities to specific major histocompatibility complex class I (MHC-I) haplotypes. NK cells can be classified as licensed or unlicensed based on their ability or inability to bind MHC-I, respectively. The role of donor vs host MHC on their development after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is not known. Following reciprocal MHC-disparate allogeneic transplants and during de novo NK-cell recovery, depletion of the licensed and not unlicensed population of NK cells as determined by the licensing patterns of donor MHC-I haplotypes, resulted in significantly increased susceptibility to murine cytomegalovirus (MCMV) infection. A corresponding expansion of the licensed Ly49H(+) NK cells occurred with greater interferon γ production by these cells than unlicensed NK cells in the context of donor MHC-I. Thus, NK licensing behavior to MCMV corresponds to the donor, and not recipient, MHC haplotype after allo-HSCT in mice.
UR - http://www.scopus.com/inward/record.url?scp=84886852339&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84886852339&partnerID=8YFLogxK
U2 - 10.1182/blood-2013-02-483503
DO - 10.1182/blood-2013-02-483503
M3 - Article
C2 - 23818546
AN - SCOPUS:84886852339
VL - 122
SP - 1518
EP - 1521
JO - Blood
JF - Blood
SN - 0006-4971
IS - 8
ER -