NKp46 regulates the production of serine proteases and IL-22 in human mast cells in urticaria pigmentosa.
NKp46 (natural cytotoxic receptor 1/CD335) is expressed on natural killer cells and Th2-type innate lymphocytes. However, NKp46 expression in human mast cells has not yet been reported. Here, we explored the expression of, and possible role played by, NKp46 in such cells. NKp46 protein was expressed in human mast cells in urticaria pigmentosa principally of the tryptase-positive/chymase-negative type (MCT), but not in human non-neoplastic skin mast cells of the tryptase-positive/chymase-positive (MCTC) type. NKp46 expression was also evident in the human neoplastic mast cell line HMC1.2. NKp46 knockdown changed the phenotype of this cell line from MCT to MCTC and downregulated GrB production, but did not influence IL-22 production. An agonistic anti-NKp46 antibody upregulated production of GrB and IL-22, but did not change the MCT-like phenotype of HMC1.2 cells. NKp46 was thus involved in the production of serine proteases and IL-22 in human mast cells.
Department of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.|Human Health Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Chiyuki
C
Ueshima
Department of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Tatsuki R
TR
Kataoka
Department of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Masahiro
M
Hirata
Department of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Itsuko
I
Koyanagi
Department of Dermatology, Kyoto University Hospital, Kyoto, Japan.
Tetsuya
T
Honda
Department of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Tatsuaki
T
Tsuruyama
Division of Molecular Cell Immunology and Allergology, Advanced Medical Research Center, Nihon University Graduate School of Medical Science, Tokyo, Japan.
Yoshimichi
Y
Okayama
Human Health Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Akitoshi
A
Seiyama
Department of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Hironori
H
Haga
D000293:Adolescent; D000328:Adult; D000368:Aged; D045744:Cell Line, Tumor; D002648:Child; D002675:Child, Preschool; D053818:Chymases / Q000378:metabolism; D005260:Female; D055785:Gene Knockdown Techniques; D053804:Granzymes / Q000096:biosynthesis; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007378:Interleukins / Q000096:biosynthesis*; D008297:Male; D008407:Mast Cells / Q000378:metabolism*; D008875:Middle Aged; D055627:Natural Cytotoxicity Triggering Receptor 1 / Q000235:genetics / Q000378:metabolism*; D010641:Phenotype; D057057:Serine Proteases / Q000096:biosynthesis*; D053802:Tryptases / Q000378:metabolism; D014582:Urticaria Pigmentosa / Q000201:enzymology / Q000378:metabolism*; D055815:Young Adult; D000097043:Interleukin-22
D053818:Chymases; D053804:Granzymes; D007378:Interleukins; D055627:Natural Cytotoxicity Triggering Receptor 1; D057057:Serine Proteases; D053802:Tryptases; D000097043:Interleukin-22; C112260:NCR1 protein, human
NKp46; chymase; granzyme B; mast cell; tryptase