Marked increase in CC chemokine gene expression in both human and mouse mast cell transcriptomes following Fcepsilon receptor I cross-linking: an interspecies comparison.
Rodent mast cells (MCs) are common experimental tools but are somewhat different from their human counterparts in their responses to certain cytokines and drugs. We examined the expression of more than 10 000 distinct genes in human and mouse cultured MCs using high-density oligonucleotide probe arrays to find molecules similarly regulated and expressed by the 2 MC types. After stimulation via high-affinity Fcepsilon receptor I (FcepsilonRI), the transcriptional levels of several CC chemokines were markedly increased, and I-309 (CCL1), macrophage inflammatory protein-1alpha (MIP-1alpha) (CCL3) and MIP-1beta (CCL4) were found among the 10 most increased human and mouse transcripts from approximately 12 000 genes (including some expressed sequence tags). In addition, a costimulatory molecule that was originally found on the membrane of activated T cells, 4-1BB (CD137), was found among the 10 most increased transcripts. The FcepsilonRI-induced expression of CC chemokines and 4-1BB was also detected at the protein level in both MC types. The conservation of these responses suggests that MCs play a crucial role in recruitment of various CCR-expressing cells into the tissue in a manner dependent on immunoglobin E, and that FcepsilonRI-mediated induction of several CC chemokines and 4-1BB is highly conserved between human and mouse. Interspecies comparison studies at the whole genome expression level should be useful for the interpretation of experimental data obtained in animal models of human pathobiology.
Nakajima
Toshiharu
T
Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan.
Inagaki
Naoki
N
Tanaka
Hiroyuki
H
Tanaka
Akane
A
Yoshikawa
Mamoru
M
Tamari
Mayumi
M
Hasegawa
Koichi
K
Matsumoto
Kenji
K
Tachimoto
Hiroshi
H
Ebisawa
Motohiro
M
Tsujimoto
Gozoh
G
Matsuda
Hiroshi
H
Nagai
Hiroichi
H
Saito
Hirohisa
H
D000818:Animals; D015703:Antigens, CD; D054402:Chemokine CCL1; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D019742:Chemokines, CC / Q000096:biosynthesis / Q000235:genetics*; D020869:Gene Expression Profiling; D006801:Humans; D019402:Macrophage Inflammatory Proteins / Q000235:genetics; D008407:Mast Cells / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D017455:Receptors, IgE / Q000378:metabolism* / Q000502:physiology; D017475:Receptors, Nerve Growth Factor / Q000235:genetics; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics; D053261:Tumor Necrosis Factor Receptor Superfamily, Member 9; D015854:Up-Regulation
D015703:Antigens, CD; C065971:CCL1 protein, human; C502258:Ccl1 protein, mouse; D054402:Chemokine CCL1; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D019742:Chemokines, CC; D019402:Macrophage Inflammatory Proteins; D012333:RNA, Messenger; D017455:Receptors, IgE; D017475:Receptors, Nerve Growth Factor; D018124:Receptors, Tumor Necrosis Factor; C505714:TNFRSF9 protein, human; C505715:Tnfrsf9 protein, mouse; D053261:Tumor Necrosis Factor Receptor Superfamily, Member 9