Disease relevance of IGKV7-3

• This line is positive for EBV DNA and expresses surface OKT11, OKT4, and Tac receptors, but not M-1, mu immunoglobulin chains, EBV receptors, or B-1 surface markers [1].
• These included antibodies to B1 and B2, both expressed exclusively on B lymphocytes, but with the latter probably restricted to a narrow window of differentiation, BB-1 and LB-1, both markers of activated lymphocytes, and 38.13, a monoclonal antibody raised against and recognizing an epitope expressed on Burkitt lymphoma cells [2].
• No significant correlation was demonstrated between the enzyme activities and histological figures (stroma amounts, etc.). Lung adenocarcinoma and squamous cell carcinoma showed the presence of an additional arylsulfatase component (B1) which was not detected in normal human lung [3].
• Different Burkitt's lymphoma lines bear one or more of a group of markers, including common acute lymphoblastic leukemia antigen gp26 (glycoprotein with a molecular weight of 26,000), B1, surface membrane immunoglobulin, HLA, beta 2-microglobulin, and Ia [4].
• Lymphomas from 28 patients (31%) did not express immunoglobulin or T-cell antigens but commonly expressed the B-lineage antigen B1; and the remaining 9 cases generally expressed Ia antigens, common ALL antigens, or both [5].

High impact information on IGKV7-3

• Plasma cells that result from antigen activation of B-1 and marginal zone B cells provide the first, rapid response to antigen [6].
• This potentially dangerous repertoire is also useful, as B-1 cells are essential for resistance to several pathogens and they play an important role in mucosal immunity [7].
• The high-resolution three-dimensional structure of a single immunoglobulin binding domain (B1, which comprises 56 residues including the NH2-terminal Met) of protein G from group G Streptococcus has been determined in solution by nuclear magnetic resonance spectroscopy on the basis of 1058 experimental restraints [8].
• In addition, B-1 cells have been implicated in autoimmunity in several murine and human studies [9].
• After 3 days in the presence or absence of TPA, these cell lines were examined morphologically, and their 5'-NT activity, Ig secretion, surface Ig, and Ia, B1, and B2 antigens were estimated [10].

Biological context of IGKV7-3

• According to its sequence B1 is a pseudogene which does not fit well into the present subgroup classification [11].
• B-1 cells (CD5+ B cells) can be distinguished from conventional B cells on the basis of phenotype, cytokine secretion, gene expression, anatomical location, and function [9].
• There was no relationship between patterns of enzyme expression in the cell lines and immunoglobulin (Ig) secretion, chromosome constitution, proliferative rate, cell volume, or the presence of B1 and B2 antigens [12].
• On the other hand, a complete search for B cell-related markers (BA-1 and B1 monoclonal antibodies, as well as cytoplasmic immunoglobulins [CyIg]) in the cALL cases showed that at least one B cell marker could be detected either on primary or on TPA-induced cells in all cases in which a gene rearrangement had occurred [13].
• One cell-specific and three ubiquitous nuclear proteins bind in vitro to overlapping motifs in the domain B1 of the SV40 enhancer [14].

Anatomical context of IGKV7-3

• In lymphoid cell lines the B1 gene region is frequently deleted [11].
• These studies suggest that a discrete maturation step occurs among CALLA-positive marrow lymphoid cells, resulting in the loss of TdT and MY10 expression, but gradual acquisition of the B cell marker B1 and the common leukocyte antigen [15].
• B-1 labeled 80%-90% of the germinal center cells and 10%-50% of the mantle region [16].
• Monoclonal antibodies OKT3, OKT4, OKT6, and OKT8 exhibited T-cell lineage restriction; and monoclonal antibodies OKB2, BL1, and B1 exhibited B-cell lineage restriction [17].
• The B1 molecule is a 32,000 m.w. phosphorylated cell surface protein expressed exclusively by B cells from the mid pre-B until the plasma cell stage of differentiation [18].

Associations of IGKV7-3 with chemical compounds

• Dual fluorescence experiments further confirmed that HCL splenocytes that coexpressed B1 and PCA-1 demonstrated both the morphology and tartrate-resistant acid phosphatase positivity of hairy cells [19].
• All five deuterium relaxation rates have been measured for deuterons in the methyl groups of the B1 immunoglobulin binding domain of peptostreptococcal protein L and the N-terminal SH3 domain from the protein drk [20].
• Activin treatment alone altered the transcriptional profile of 303 genes including inducing that of the 17beta-hydroxysteroid dehydrogenase B1 gene that converts estrone to 17beta-estradiol, altering the sensitivity of the cells to estrone [21].
• The Kd for hVII-B101/B1 to FVII was 1.75 x 10(-10) M in the presence of 5 mM CaCl2 [22].
• The actions of bradykinin (BK) in mammals are mediated through the activation of the B1 and B2 BK receptors [23].

Analytical, diagnostic and therapeutic context of IGKV7-3

• We have used the gel retardation assay to investigate the binding of nuclear proteins to the domain B1 of the SV40 enhancer, which contains the GT-II motif [14].
• METHODS: In the present study we investigated B cell subsets (i.e., the CD5(+) B-1 and CD5- B-2 subsets) by flow cytometric analysis, and their subclasses of antibody, by ELISA, in patients who had undergone renal transplantation across the blood barrier [24].
• CONCLUSIONS: The results of this study suggested that CD5(+) B-1 cell T-independent activation usually occurs soon after ABO-incompatible renal transplantation, but that CD5- B-2 cell T-dependent activation occurs only in patients who experience graft rejection [24].
• RESULTS: The B-cell population analysis revealed that CD5(+) B-1 cells temporarily increased in all patients in both groups soon after transplantation, and that CD5- B-2 cells significantly increased 1 month after transplantation only in group 2 [24].
• The real-time PCR assay with new alternative targets to the B1 gene may have potential for monitoring the clinical outcome of disease and for providing molecular information regarding the actual state of infection [25].

References