Disease relevance of DEFA6

• Unlike hBDs, only low levels of HD5 and HD6 were detectable in papillomas and in oral mucosa [1].
• To test if levels of defensin expression are altered in NEC, specimens from six cases of patients with NEC and five control subjects (four patients with atresia and one with meconium ileus) were analyzed to determine HD5 and HD6 mRNA levels by in situ hybridization [2].
• Helicobacter pylori had no impact on the gastric expression of HD-5 and HBD-1, whereas HD-6 was increased in the fundus [3].
• A library of recombinant bacteriophage was prepared from ts167 avian erythroblastosis virus-transformed erythroid precursor cells (HD6), and integrated proviruses from three distinct genomic loci were isolated [4].
• Analysis of immunological markers by flow cytometry revealed that the monoclonal antibody defined cell surface molecule HD6 (CD22), which is strongly expressed on hairy cell leukemia (HCL) but absent from plasmacytoma and plasma cells, can be induced or enhanced in the leukemic samples [5].

High impact information on DEFA6

• Paneth cells (PC) are the major source of antimicrobial peptides in the small intestine, including human alpha-defensins HD5 and HD6 [6].
• HSF3 is constitutively expressed in the erythroblast cell line HD6, the lymphoblast cell line MSB, and embryo fibroblasts, and yet its DNA-binding activity is induced only upon exposure of HD6 cells to heat shock [7].
• The DNA-binding properties of two heat shock factors, HSF1 and HSF3, are induced in the avian erythroblast cell line HD6 [7].
• Ricin A chain-containing immunotoxins (IT-As) specific for the human B-cell antigens, CD22 and CD19, were constructed using the monoclonal antibodies, HD6 and HD37, respectively [8].
• Neither HD6 nor HD37 IT-As affected the ability of normal human bone marrow cells to form granulocyte-macrophage colony-forming units in soft agar, suggesting that both antigens are absent from these progenitor cells [8].

Biological context of DEFA6

• HD-6 mRNA was detectable at 13.5-17 weeks of gestation in the small intestine but not in the colon [9].
• Analysis of a panel of human/hamster hybrids localized both HD-5 and HD-6 to chromosome 8 [10].
• Polarization is an early event in HD6 cell differentiation, with the polarized cells forming a tight, laterally adherent monolayer by culture in normal calcium medium [11].

Anatomical context of DEFA6

• In this study, we determined the chromosomal localization of the human defensin (HD) genes expressed in Paneth cells, HD-5 and HD-6 [10].
• Human alpha defensins (HD-5 and HD-6) are antibiotic effector molecules predominantly expressed in Paneth cells of the ileum [12].
• We describe the isolation of naturally occurring human intestinal defensins HD-5 and HD-6 from ileal neobladder urine and ileal mucosa [13].
• We compared the expression of human alpha- and beta-defensins by various human tissues. mRNA for alpha-defensins HNP1-3, abundant in bone marrow, was detected in peripheral blood leukocytes, spleen and thymus by RT-PCR, which revealed alpha-defensins HD5 and HD6 only in the small intestine [14].
• HNP-1, HD-5, and HD-6 were present in significantly higher levels in colostrum than in mature milk [15].

Associations of DEFA6 with chemical compounds

• SLED consisted of 8 h of HD 6 days a week, with blood flow of 200 ml/min, dialysate flows of 350 ml/min, and hemofiltration with 1 l of saline/h. CRRT patients were anticoagulated with either heparin or citrate, and SLED patients with either heparin or saline flushes [16].
• Polarized HD6 cells exhibit low levels of CEA only at their apical luminal surface [11].

Other interactions of DEFA6

• The natural antimicrobial defensin DEFA5 and DEFA6 genes were particularly over-expressed in CD [17].

Analytical, diagnostic and therapeutic context of DEFA6

• The two isoforms detected by this PCR approach were human defensin family members, HD-5 and HD-6 [9].
• The initial dialysis (HD1) was performed with a low flux polysulfone dialyzer, the following dialyses (up to HD6) with a high flux polysulfone dialyzer and regular heparin [18].
• We report the case of a eight-year-old girl who developed HD 6 years after treatment for common acute lymphoblastic leukemia (ALL) [19].
• In spite of this the proportion of patients receiving the chemotherapy on in-patient departments is 54% per chemotherapy cycle in average in the HD6 trial for advanced Hodgkin's disease of the German Hodgkin Study Group (GHSG) [20].
• TPA treatment induced a greatly enhanced HD 6 binding in CLL and IC cells compared to controls as demonstrated by indirect immunofluorescence [21].

References