Modulation of natural killer (NK) receptors on NK (CD3-/CD56+), T (CD3+/CD56-) and NKT-like (CD3+/CD56+) cells after heart transplantation.
BACKGROUND
After undergoing heart transplantation and the subsequent compulsive immunosuppressive treatments, patients are at risk of rejection episodes, infectious complications or cancer development. Thus, it is probable that the various subsets of peripheral cytotoxic lymphocytes are modulated in such patients. This area of study can now be investigated by examining the numerous recently described natural killer (NK)-cell-related surface receptors.


METHODS
A prospective cohort of 60 heart transplant recipients and 60 controls was studied. The partitioning of lymphocyte subsets, especially NK (CD3-/CD56+), T (CD3+/CD56-) and NKT-like (CD3+/CD56+) cells, was compared in both groups using multi-parametric flow cytometry. Moreover, expression of a series of seven NK-related receptors was compared on the three subsets defined by CD56 expression.


RESULTS
A significant increase in NK-cell levels was observed in transplanted patients, as compared with controls, whereas T and NKT-like cells were in similar proportions in both groups. Two NK-related receptors showed significantly different levels of expression in heart transplant recipients: the cytotoxic effector, CD244, which was in a significantly increased proportion on T and NKT-like cells; and the activating receptor, CD161, which was expressed significantly less on NK and NKT-like cells, but more on T cells.


CONCLUSIONS
These findings indicate that cytotoxic NK-related cells, increased in proportion, also display increased levels of activity-associated markers in heart transplant recipients. Viral infection or the immunosuppressive regimen could be responsible for the modulation of regulatory receptors on NK and NKT-like cells in heart transplant recipients.
Aguilar
Patricia
P
Immunology Laboratory, Faculty of Medicine and CHU, BP184, Nancy, France. bene@medecine.uhp-nancy.fr
Mathieu
Christine Prin
CP
Clerc
Georges
G
Ethevenot
Gerard
G
Fajraoui
Mohamed
M
Mattei
Sophie
S
Faure
Gilbert C
GC
Bene
Marie C
MC
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000032:analysis; D000954:Antigens, Surface / Q000032:analysis; D017252:CD3 Complex / Q000032:analysis; D019002:CD56 Antigen / Q000032:analysis; D016022:Case-Control Studies; D005260:Female; D006084:Graft Rejection / Q000276:immunology / Q000473:pathology; D016027:Heart Transplantation / Q000276:immunology* / Q000473:pathology / Q000502:physiology; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology / Q000627:therapeutic use; D007239:Infections / Q000276:immunology / Q000473:pathology; D007694:Killer Cells, Natural / Q000737:chemistry* / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D037181:Lectins, C-Type / Q000032:analysis; D016131:Lymphocyte Subsets / Q000737:chemistry / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011446:Prospective Studies; D011971:Receptors, Immunologic / Q000032:analysis* / Q000187:drug effects / Q000502:physiology; D055607:Receptors, Natural Killer Cell; D000071176:Signaling Lymphocytic Activation Molecule Family; D013601:T-Lymphocytes / Q000737:chemistry* / Q000187:drug effects / Q000276:immunology* / Q000473:pathology
D015703:Antigens, CD; D000954:Antigens, Surface; C084093:CD244 protein, human; D017252:CD3 Complex; D019002:CD56 Antigen; D007166:Immunosuppressive Agents; C527203:KLRB1 protein, human; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011971:Receptors, Immunologic; D055607:Receptors, Natural Killer Cell; D000071176:Signaling Lymphocytic Activation Molecule Family