Disease relevance of KIR3DL2

• Only scattered CD8+ cells in lichen planus expressed a significant amount of KIR3DL2 [1].
• p140/KIR3DL2 has been identified in malignant cell lines isolated from the skin and blood of patients with transformed mycosis fungoides (MF) and Sézary's syndrome (SS) [1].
• CD158k/KIR3DL2 is a new phenotypic marker of Sezary cells: relevance for the diagnosis and follow-up of Sezary syndrome [2].
• Other established human hepatoma and hepatoblastoma cell lines, HuH-6 cl-5, PLC/PRF/5, huH-1, and huH-4, also grew in the defined medium [3].
• This study has determined the ability of MEP to alter the expression of select genes from drug metabolism, cytokine, oncogene, tumor suppressor, and estrogen signaling families of human lung adenocarcinoma CL5 cells. cDNA microarray analyses and confirmation studies were performed using CL5 cells treated with 100 microg/ml MEP extract for 6 h [4].

High impact information on KIR3DL2

• Polymorphic expression of CD158k/p140/KIR3DL2 in Sézary patients [5].
• We previously found that CTCL malignant cells express the killer cell immunoglobulinlike receptor (KIR) KIR3DL2/CD158k, whereas they fail to express the other KIRs [6].
• Three particular receptors, KIR2DS2, KIR2DL2, and KIR3DL2, had significant differences in gene expression frequencies between the clone families [7].
• KIR3DL1 and KIR3DL2 are NK cell receptors for polymorphic HLA-B and -A determinants [8].
• Functional and molecular characterization of a KIR3DL2/p140 expressing tumor-specific cytotoxic T lymphocyte clone infiltrating a human lung carcinoma [9].

Biological context of KIR3DL2

• Strikingly, both the lytic and the cytokine secretion activities induced upon specific cell interactions were unaffected by anti-KIR3DL2/p140 antibody [9].
• Single amino acid substitutions in the nonamer peptide underline a critical role for residue 8 in recognition of KIR3DL2 [10].
• We observed 18 different genotypes and eight KIR3DL2 alleles in the population, with KIR3DL2*002 having the highest frequency of 0.558, and confirmed the new KIR3DL2*015 allele [11].
• Additionally, the KIR3DL2 allele status of cell line DNA and Centre d'Etude du Polymorphisme Humain (CEPH) families, both from the 13th International Histocompatibility Workshop, has been established [12].
• Our data showed that the established PCR-SBT methods for KIR3DL2 allele typing were reliable, and Chinese Han population is distinct in KIR3DL2 allele frequencies [11].

Anatomical context of KIR3DL2

• Alternatively, KIR3DL2 was detected on TALL-104, and expression of its reported ligand, human leukocyte antigen (HLA)-A, on target cells provided protection from cytotoxicity [13].
• In contrast, MEP decreased tumor suppressor Rb mRNA in CL5 lung epithelial cells [4].
• Incubation of human lung fibroblast WI-38 with MEP- or benzo(a)pyrene-induced CL5 conditioned medium for 4 days stimulated cell growth of the fibroblasts [4].
• Analysis of the CGD samples by immunoblotting indicated that CL5 recognizes only the full-length wild-type and two missense mutations, consistent with the absence of stable short gp91phox peptide expression in CGD neutrophils [14].
• The presence of microvilli can be controlled as a function of temperature by two temperature-sensitive mutants of the Kirsten sarcoma virus (ts6t6 and ts371 cl 5) [15].

Other interactions of KIR3DL2

• Extension of this comparative analysis to include all 12 KIR family members showed that KIR2DL3 and KIR3DL2 were the only genes whose transcripts were consistently detectable [16].

Analytical, diagnostic and therapeutic context of KIR3DL2

• 2. Sequence analysis indicated that KIR3DL2/p140 cDNA was identical to the previously reported 3DL2*002 allele except for two nucleic acid substitutions [9].

References