Antigenic Phenotyping of Lymphoid Cells and B Cell Gene Rearrangement in Type B Gastritis and in Gastritis Not Associated with Helicobacter pylori Colonization

1999 ◽  
Vol 102 (2) ◽  
pp. 77-82 ◽  
Author(s):  
A. Fritscher-Ravens ◽  
S. Petrasch ◽  
M. Tiemann ◽  
H. Wacker ◽  
T. Dörr ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
B Cell ◽  
Gene Rearrangement ◽  
Lymphoid Cells ◽  
Type B ◽  
Type B Gastritis ◽  
Cell Gene

scholarly journals Inhibition of immunoglobulin gene rearrangement by the expression of a lambda 2 transgene.

1989 ◽  
Vol 169 (6) ◽  
pp. 1911-1929 ◽  
Author(s):  
J Hagman ◽  
D Lo ◽  
L T Doglio ◽  
J Hackett ◽  
C M Rudin ◽  
...  
Keyword(s):  
B Cells ◽  
Transgenic Mice ◽  
B Cell ◽  
Gene Rearrangement ◽  
Feedback Inhibition ◽  
Cell Lineage ◽  
Serum Levels ◽  
Lymphoid Cells ◽  
Immunoglobulin Gene ◽  
Cell Stage

The rearrangement of Ig genes is known to be regulated by the production of H and kappa L chains. To determine whether lambda L chains have a similar effect, transgenic mice were produced with a lambda 2 gene. It was necessary to include the H chain enhancer, since a lambda gene without the added enhancer did not result in transgene expression. The lambda 2 transgene with the H enhancer was expressed in lymphoid cells only. The majority of the B cells of newborn transgenic mice produced lambda, whereas kappa + cells were reduced. Concomitantly, serum levels of kappa and kappa mRNA were diminished. By 2 wk after birth the proportion of kappa-expressing cells was dramatically increased. Adults had reduced proportions of B cells that produced lambda only, but the levels of lambda were still higher than in normal littermates. Also, kappa + cells were still lower than in normal mice. Analysis of hybridomas revealed that reduction of kappa gene rearrangement was the basis for the decreased frequency of kappa + cells. Furthermore, many cells also contained an unrearranged H chain allele. It was concluded that feedback inhibition by the lambda 2 together with endogenous H protein may have inhibited recombinase activity in early pre-B cells, leading to inhibition of both H chain and kappa gene rearrangement. Thus, lambda 2 can replace kappa in a feedback complex. The levels of serum lambda 1 and, to a lesser degree, of spleen lambda 1 mRNA were reduced in the lambda 2 transgenic mice. However, the proportion of hybridomas with endogenous lambda gene rearrangement was at least as high as in normal mice. It was therefore concluded that the suppression of functional lambda 1 may be a consequence of decreased selection of endogenous lambda-producing cells because of the excess of transgenic lambda. The escape of kappa-producing cells from feedback inhibition may be the result of several mechanisms that operate to varying degrees, among them: (a) kappa rearrangement during a period in which the recombinase is still active after appearance of a lambda 2/mu stop signal; (b) a B cell lineage that is not feedback inhibited at the pre-B cell stage; (c) subthreshold levels of transgenic lambda 2 in some pre-B cells; and (d) loss of the lambda 2 transgenes in rare pre-B cells.

CD15+ Acute Lymphoblastic Leukemia and Subsequent Monoblastic Leukemia

2001 ◽  
Vol 125 (9) ◽  
pp. 1227-1230
Author(s):  
Cherie H. Dunphy ◽  
Laura J. Gardner ◽  
H. Lance Evans ◽  
Nader Javadi
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Progenitor Cell ◽  
Gene Rearrangement ◽  
Chromosomal Abnormalities ◽  
Lymphoblastic Leukemia ◽  
Enzyme Cytochemistry ◽  
Flow Cytometric ◽  
Additional Chromosomal Abnormalities ◽  
Cell Gene

Abstract The abnormality in the translocation of chromosomes 4 and 11 (t[4;11]) has been characteristically associated with calla-negative CD15+ acute lymphoblastic leukemia (ALL) of early pre–B-cell origin. Transformation of a lymphoblastoid to a monoblastoid morphologic structure has rarely been described at relapse in these cases; however, these cases have lacked flow cytometric immunophenotyping (FCI) and genotypic studies (GS) to define the immunophenotype of and the presence of a B-cell gene rearrangement in the monoblastoid component. We report a case of CD15+, CD10− ALL of early pre–B-cell origin defined by morphologic testing and FCI with the t(4;11) abnormality. At relapse, the morphologic testing, enzyme cytochemistry, and FCI data were characteristic of monoblastic leukemia. The t(4;11) abnormality persisted with associated additional chromosomal abnormalities, and the monoblasts contained a B-cell gene rearrangement by GS. These findings support the concept that both processes arose from a multipotential progenitor cell.

B-cell gene rearrangement in benign and malignant lymphoid proliferations of mucosa-associated lymphoid tissue and lymph nodes

1997 ◽  
Vol 28 (2) ◽  
pp. 166-173 ◽  
Author(s):  
Emina Torlakovic ◽  
David L Cherwitz ◽  
Jose Jessurun ◽  
John Scholes ◽  
Ronald McGlennen
Keyword(s):  
Lymph Nodes ◽  
B Cell ◽  
Lymphoid Tissue ◽  
Gene Rearrangement ◽  
Cell Gene

scholarly journals Understanding Disease Outcome Following Acquisition ofHelicobacter pyloriInfection during Childhood

1999 ◽  
Vol 13 (3) ◽  
pp. 229-234 ◽  
Author(s):  
Andrew S Day ◽  
Philip M Sherman
Keyword(s):  
Helicobacter Pylori ◽  
Virulence Factors ◽  
Peptic Ulceration ◽  
Host Responses ◽  
Type B ◽  
Microbial Infection ◽  
Active Type ◽  
Relative Contribution ◽  
The Subject ◽  
Type B Gastritis

Helicobacter pyloricauses chronic active (type B) gastritis in the overwhelming majority of infected individuals. The relative contribution of virulence factors in the bacterium and host responses to the microbial infection in determining which subjects will go on to develop complications–such as peptic ulceration, gastric cancers and gastric lymphomas—is the subject of current investigative activities.

scholarly journals Theory of Additional Corpus Biopsy for Epidemiology and Diagnosis of Helicobacter Pylori

2017 ◽  
Vol 1 (1) ◽  
pp. 01-04
Author(s):  
Vijay Kumar Bontha ◽  
Swathi Goli ◽  
Prasad Garrepally
Keyword(s):  
Helicobacter Pylori ◽  
Acute Infection ◽  
Colorectal Polyps ◽  
Campylobacter Pylori ◽  
Causative Role ◽  
Type B ◽  
Ulcer Disease ◽  
Acute Gastritis ◽  
H Pylori ◽  
Type B Gastritis

Background: There is still debate on the best sites for biopsy- based tests of Helicobacter pylori infection in patients with gastritis. This study was designed to determine if it is important to add corpus biopsies to the routine antral ones for identification of H. pylori, especially in case of gastric atrophy and/or intestinal metaplasia. Methods: A causative role is now accepted for Helicobacter (formerly Campylobacter) pylori in type B gastritis, and evidence is accumulating that H. pylori infection plays a major contributory role in peptic ulcer disease. Preliminary studies have reported that the prevalence of H pylori infection increases with age, but detailed information on the prevalence of the bacteria in any defined population and on the factors that may influence the pattern of distribution remains scanty. Results: Up to 85% of people infected with H. pylori never experience symptoms or complications. Acute infection may appear as an acute gastritis with abdominal pain (stomach ache) or nausea. Where this develops into chronic gastritis, the symptoms, if present, are often those of nonulcer dyspepsia: stomach pains, nausea, bloating, belching, and sometimes vomiting or black stool. Conclusion: H. pylori has been associated with colorectal polyps and colorectal cancer. It may also be associated with eye disease.

scholarly journals Use of B Cell Gene Rearrangement Studies to Establish Clonality in Cases of Nonproducer Nonsecretory Multiple Myeloma

2013 ◽  
Vol 140 (suppl 1) ◽  
pp. A220-A220
Author(s):  
Alexa Siddon ◽  
Richard Torres ◽  
Christopher Tormey
Keyword(s):  
Multiple Myeloma ◽  
B Cell ◽  
Gene Rearrangement ◽  
Cell Gene

Use of B-Cell Gene Rearrangement Studies to Establish Clonality in Non-producer Non-secretory Multiple Myeloma

2020 ◽  
Vol 20 (1) ◽  
pp. e18-e21
Author(s):  
Hadrian Mendoza ◽  
Christopher A. Tormey ◽  
Alexa J. Siddon
Keyword(s):  
Multiple Myeloma ◽  
B Cell ◽  
Gene Rearrangement ◽  
Cell Gene

Lymphoproliferative disorders (LPD) involving lungs: T and B cell subsets within pulmonary infiltrates and in peripheral blood

1984 ◽  
Vol 42 ◽  
pp. 700-701
Author(s):  
Irene Stachura ◽  
Milton H. Dalbow ◽  
Michael J. Niemiec ◽  
Matias Pardo ◽  
Gurmukh Singh ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Lymphoproliferative Disorders ◽  
Mixed Population ◽  
Lymphoid Cells ◽  
Lymphomatoid Granulomatosis ◽  
Cell Type ◽  
Cell Surface Antigens ◽  
Pulmonary Infiltrates ◽  
B Cell Subsets

Lymphoid cells were analyzed within pulmonary infiltrates of six patients with lymphoproliferative disorders involving lungs by immunofluorescence and immunoperoxidase techniques utilizing monoclonal antibodies to cell surface antigens T11 (total T), T4 (inducer/helper T), T8 (cytotoxic/suppressor T) and B1 (B cells) and the antisera against heavy (G,A,M) and light (kappa, lambda) immunoglobulin chains. Three patients had pseudolymphoma, two patients had lymphoma and one patient had lymphomatoid granulomatosis.A mixed population of cells was present in tissue infiltrates from the three patients with pseudolymphoma, IgM-kappa producing cells constituted the main B cell type in one patient. In two patients with lymphoma pattern the infiltrates were composed exclusively of T4+ cells and IgG-lambda B cells predominated slightly in the patient with lymphomatoid granulomatosis.

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