scholarly journals Genetic Control of the Radiosensitivity of Lymphoid Cells for Antibody Formation Ability in Mice.

1994 ◽  
Vol 35 (3) ◽  
pp. 179-185
Author(s):  
MASAAKI OKUMOTO ◽  
NOBUKO MORI ◽  
SHUNSUKE IMAI ◽  
SATOMI HAGA ◽  
JO HILGERS ◽  
...  
Keyword(s):  
Genetic Control ◽  
Antibody Formation ◽  
Lymphoid Cells

scholarly journals GENETIC CONTROL OF THE IMMUNE RESPONSE

1972 ◽  
Vol 136 (5) ◽  
pp. 1195-1206 ◽  
Author(s):  
John C. Ordal ◽  
F. Carl Grumet
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Genetic Control ◽  
Antibody Production ◽  
Lymphoid Cells ◽  
Antigen Challenge ◽  
Graft Versus Host ◽  
K Cells

The transfer of parental (H-2k/k) nonresponder lymphoid cells into heterozygous (H-2k/q) nonresponder recipients at the time of primary challenge with aqueous poly-L(Tyr,Glu)-poly-D,L-Ala-poly-L-Lys [(T,G)-A--L] elicited the production of both IgM and IgG anti-(T,G)-A--L antibody. Normally, the production of IgG anti-(T,G)-A--L antibody is restricted to strains possessing the responder Ir-1 allele. The timing and intensity of the graft-versus-host (GVH) reaction required for this effect were found to be critical. Injection of H-2k/k cells into H-2k/q recipients 1 wk before antigen challenge did not elicit IgG anti-(T,G)-A--L antibody production, and markedly suppressed IgM anti-(T,G)-A--L antibody production. The transfer of alloimmune (H-2q-primed) H-2k/k cells at the time of antigen challenge was also associated with no IgG and little IgM anti-(T,G)-A--L antibody production. These data are consistent with the model that nonresponder thymus-derived lymphocytes (T cells) activated in a GVH reaction can substitute for (T,G)-A--L-reactive T cells to induce a shift from IgM to IgG anti-(T,G)-A--L antibody production.

The genetic control of antibody formation

1983 ◽  
Vol 4 (1-2) ◽  
pp. 3-42
Author(s):  
Rochelle K. Seide ◽  
J. Michael Kehoe
Keyword(s):  
Genetic Control ◽  
Antibody Formation

scholarly journals THE NATURE OF THE IMMUNOLOGIC INADEQUACY OF NEONATAL RABBITS

1959 ◽  
Vol 110 (1) ◽  
pp. 139-146 ◽  
Author(s):  
Frank J. Dixon ◽  
William O. Weigle
Keyword(s):  
Antibody Formation ◽  
Lymphoid Cells

It has been shown that cells from neonatal rabbits are capable of producing considerable amounts of antibody after exposure to antigen in vitro and transfer to x-radiated adult recipients. This suggests that the immunological inadequacy of these neonates is not dependent primarily upon the lack of cells capable of antibody formation. Both in vitro sensitized neonatal lymphoid cells and in vivo sensitized adult lymphoid cells made much more antibody after transfer to x-rayed adult recipients than to neonatal recipients. Possible reasons for and significance of these observations are pointed out in the discussion.

scholarly journals THE EFFECTS OF MERCAPTOETHANOL AND OF PERITONEAL MACROPHAGES ON THE ANTIBODY-FORMING CAPACITY OF NONADHERENT MOUSE SPLEEN CELLS IN VITRO

1972 ◽  
Vol 136 (3) ◽  
pp. 604-617 ◽  
Author(s):  
Chang Chen ◽  
James G. Hirsch
Keyword(s):  
Antibody Formation ◽  
Peritoneal Macrophages ◽  
Lymphoid Cells ◽  
Red Cells ◽  
Mouse Spleen ◽  
Spleen Cells ◽  
Sheep Red Cells ◽  
Low Concentrations ◽  
Nonadherent Cells

Nonadherent mouse spleen cells exhibited poor viability and little or no capacity to form antibodies to sheep red cells in the Mishell-Dutton culture system. Viability and antibody-forming capacity could be restored by addition to these cultures of low concentrations of mercaptoethanol (10–4–10–5 M), or by addition of appropriate numbers of mouse peritoneal macrophages. Macrophage concentrations lower than optimal resulted in lower lymphoid cell viability and correspondingly fewer plaque-forming cells, whereas excess macrophages resulted in marked inhibition of antibody formation despite good viability of the lymphocytes. Restoration of the nonadherent cells with mercaptoethanol was thus much simpler and more reproducible than it was with macrophages; furthermore, the number of plaque-forming cells developed in cultures restored with mercaptoethanol was approximately fourfold higher than it was in cultures restored with optimal numbers of macrophages. In the presence of mercaptoethanol, the plaque-forming capacity of the nonadherent spleen cells was not increased when small numbers of macrophages were added to the system, nor was it decreased when the few macrophages present in the nonadherent cells were further reduced or eliminated. Excess macrophages inhibited antibody formation in the cultures containing mercaptoethanol as they did in control cultures. Optimal restoration of plaque-forming capacity to the nonadherent spleen cells with mercaptoethanol required the reducing agent to be present throughout the 4 or 5 day culture period. Addition of mercaptoethanol 1 or more days after initiation of culture, or transfer of the cells to a medium free of mercaptoethanol before completion of the culture resulted in a reduction in the numbers of plaque-forming cells. The results suggest that mouse lymphoid cells do not require macrophages in order to form antibodies to sheep red cells in vitro, provided mercaptoethanol is present in the culture medium. The mechanism of action of mercaptoethanol under these conditions is not completely clear, but one of its effects is to promote the viability of lymphoid cells in the cultures.

scholarly journals GENETIC CONTROL OF THE ANTIBODY RESPONSE IN INBRED MICE

1968 ◽  
Vol 128 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Hugh O. McDevitt ◽  
Marvin L. Tyan
Keyword(s):  
Genetic Control ◽  
Antibody Formation ◽  
Inbred Mice ◽  
Progeny Testing ◽  
Secondary Immune Response ◽  
Linkage Studies ◽  
Spleen Cells ◽  
The Third ◽  
Backcross Populations ◽  
Synthetic Polypeptide

The transfer of spleen cells from (C3H x C57Bl/6) F1 mice, capable of responding to (T,G)-A--L, into irradiated C3H parental recipients, normally incapable of responding to (T,G)-A--L, transfers the ability to make either a primary or secondary immune response to this synthetic polypeptide antigen. This localizes the genetic control of the ability to respond to the spleen cell population and indicates that the genetic control is exerted upon a process directly related to antibody formation. Studies with congenic strains of mice and linkage studies in segregating backcross populations show that the ability to respond to (T,G)-A--L and (H,G)-A--L is linked to the H-2 locus and can thus be localized to the IXth mouse linkage group. Note Added in Proof: Of the three possible recombinant animals noted in Tables IV and V, two were infertile. The third animal was not a recombinant, since progeny testing and reimmunization showed that this animal was an H-22/H-2k heterozygote capable of responding well to (T,G)-A--L.

Genetic control of immunoglobulin synthesis

1970 ◽  
Vol 176 (1044) ◽  
pp. 329-346 ◽  
Keyword(s):  
Genetic Control ◽  
Mammalian Species ◽  
Variable Region ◽  
Lymphoid Cells ◽  
The Other ◽  
Light Chains ◽  
Common Region ◽  
Variable Regions ◽  
Immunoglobulin Synthesis ◽  
Heavy Chains

The structural features of immunoglobulins are described. This family of related proteins shows a common structural design: two identical light chains and two identical heavy chains are present in each molecule. Amino acid sequence studies have shown that light chains have one of two types of sequences in the C terminal half, whereas they differ one from the other in the N terminal half. The two halves of the sequence have been designated accordingly variable and common half. Similarly, the heavy chains have a common sequence in the C terminal three-quarters of the sequence and a variable one in the N terminal quarter. Genetic studies on the inheritance of immunoglobulin alleles have been carried out in some mammalian species. The genetic control of immunoglobulin synthesis is reviewed in man, mouse and rabbit. These studies have shown that each allele controls the inheritance of a specific common region, with the exception of one genetic system which seems to control the synthesis of the variable region of rabbit heavy chains. Immunoglobulin chains are clearly synthesized under the control of two distinct genetic elements, one of which specifies the variable region and the other the common region. The possible significance of this type of genetic control of immunoglobulin structure is discussed. It has not yet been established whether each variant of the variable region is coded for by an individual structural gene present in the genome of each individual or whether few genes for variable regions exist, which in the course of the differentiation of lymphoid cells are subject to somatic mutation processes, which generate variability. These two possibilities are discussed and elements in favour of one or the other theory are presented.

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.

Sign in / Sign up

Export Citation Format

Share Document