scholarly journals T-helper Activity at Women Nadym of YaNAO

2018 ◽  
Vol 15 (2) ◽  
pp. 248-255 ◽  
Author(s):  
M.S. Kabbani ◽  
L.S. Shchegoleva
Keyword(s):  
T Helper ◽  
Helper Activity

scholarly journals An idiotype-specific helper population that bears immunoglobulin, Ia, and Lyt-1 determinants.

1984 ◽  
Vol 159 (4) ◽  
pp. 1189-1200 ◽  
Author(s):  
D H Sherr ◽  
M E Dorf
Keyword(s):  
T Cells ◽  
B Cells ◽  
Cell Population ◽  
T Helper Cells ◽  
T Helper ◽  
Phenotypic Characteristics ◽  
Surface Phenotype ◽  
Specific Recognition ◽  
Helper Cells ◽  
Helper Activity

A helper cell population with phenotypic characteristics of both B and T cells is described. This helper population, called BH, is present in normal unprimed C57BL/6 mice and preferentially helps the expression of NPb idiotype-bearing plaque-forming B cells in the absence of T helper cells. Its surface phenotype is Lyt-1.2+, Ig+, Lyb-3+, Thy-1.2-, Lyt-2.2-. The helper activity of the BH population is IgH restricted and BH cells selectively bind NPb idiotypic determinants. Collectively the data demonstrate that this unique subpopulation can regulate the response of antibody-secreting B cells through specific recognition of idiotypic determinants.

scholarly journals Idiotypic analysis of lymphocytes in vitro. I. Specificity and heterogeneity of B and T lymphocytes reactive with anti-idiotypic antibody.

1976 ◽  
Vol 143 (4) ◽  
pp. 846-860 ◽  
Author(s):  
S J Black ◽  
G J Hämmerling ◽  
C Berek ◽  
K Rajewsky ◽  
K Eichmann
Keyword(s):  
Variable Region ◽  
Antigen Receptors ◽  
T Helper ◽  
Myeloma Protein ◽  
Immunoglobulin Molecule ◽  
Helper Activity ◽  
Group A ◽  
Idiotypic Antibody ◽  
B And T Lymphocytes

Guinea pig anti-idiotypic antibodies (anti-Id) of the IgG1 class, directed to an A/J antibody to Group A streptococcal carbohydrate (A-CHO), or directed to a BALB/c myeloma protein that binds the same antigen, stimulate B-precursor cells as well as T-helper cells when injected into mice of the appropriate strain. The strain-specific induction of both precursor and helper activity was detected by in vitro secondary responses of primed spleen cells to A-CHO or to 2,4,6-trinitrophenyl (TNP) upon challenge with Group A streptococcal vaccine (Strep.A) or with TNP-Strep.A, respectively. B- and T-cell populations primed with anti-Id were uniform with respect to the binding of antigen and of anti-Id. This was in contrast to cells primed with Strep.A, which were heterogenous. Taken together, B and T cells that possess the same antigen-binding specificity share idiotypic determinants, reveal the same idiotypic polymorphism, and may display similar degrees of heterogeneity with respect to the binding of antigen and anti-Id. Since the anti-Id used in this study detect Id determinants associated with the heavy chain of the variable region of mouse antibodies, the data suggest that this region of the immunoglobulin molecule is shared between T- and B-cell antigen receptors.

scholarly journals Two Ly-2 T helper cell subsets distinguished by Qa-1 phenotype. The priming environment determines whether one or both subsets will be generated.

1982 ◽  
Vol 155 (3) ◽  
pp. 831-838 ◽  
Author(s):  
J S McDougal ◽  
F W Shen ◽  
S P Cort ◽  
J Bard
Keyword(s):  
T Cells ◽  
B Cells ◽  
Cell Activity ◽  
T Helper Cell ◽  
T Cell Subsets ◽  
Helper Cell ◽  
T Helper ◽  
Effector Cells ◽  
Helper Activity ◽  
Effector Activity

The Qa-1 cell surface phenotype reportedly distinguishes two Ly-1 T cell subsets conjointly required for T helper effector activity. Ly-1 cells, obtained from several different priming regimens, were negatively selected with anti-Qa-1 plus complement and compared with unselected Ly-1 cells for helper cell activity. Priming isolated T cells on antigen-pulsed macrophages in the absence of B cells favors the generation of the Ly-1:Qa1- subset, which is capable of efficient helper activity in the absence of the Ly-1:Qa-1+ subset. Priming T cells in an environment containing B cells generates both Ly-1:Qa-1- helper effector cells and Ly-1:Qa-1+ cells which contribute to the helper effect. Whether Ly-1:Qa-1+ cells are capable of independent helper activity cannot be determined, and, as such, Ly-1:Qa-1+ cells are more appropriately termed "help associated" rather than "helper effector." Our results assign a membrane phenotype, Qa-1, which distinguishes an Ly-1 help-associated B cell requiring subset in our system and may prove to be a general marker in a number of systems of Ly-1 inducer cell subsets which functionally require or recognize B cells or their products.

Defective T helper activity in the spleen of BALB/c mice immune to a syngeneic fibrosarcoma

1987 ◽  
Vol 24 (3) ◽  
Author(s):  
Laura Grazioli ◽  
Marialuisa Sensi ◽  
Giorgio Parmiani
Keyword(s):  
T Helper ◽  
Helper Activity

scholarly journals Genetic control of immunoregulatory circuits. Genes linked to the Ig locus govern communication between regulatory T-cell sets.

1979 ◽  
Vol 150 (1) ◽  
pp. 44-50 ◽  
Author(s):  
D D Eardley ◽  
F W Shen ◽  
H Cantor ◽  
R K Gershon
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Surface ◽  
Regulatory T Cell ◽  
Cell Surface Molecules ◽  
Suppressive Activity ◽  
T Helper ◽  
Surface Molecules ◽  
Helper Activity ◽  
Per Se

Antigen-stimulated Ly1:Qa1+ cells induce a nonimmune set of T-acceptor cells (surface phenotype Ly123+Qa1+) to participate in the generation of specific suppressive activity. The experiments reported here were designed to test the possibility that the interaction between T-inducer and T-acceptor cells might be governed by genes linked to the Ig locus. We find that inducer:acceptor interactions occur only if the inducer and acceptor T-cell sets are obtained from donor that are identical at the Ig locus and are independent of the Ig locus expressed on the B cells used for assay of T-helper activity. In addition, experiments using inducer and acceptor T cells from the congenic recombinant BAB. 14 strain show that T-T interactions are not governed by Ig-CH genes, per se. These data indicate that T-inducer: T-acceptor interactions are governed by Ig-linked genes that may control expression of VH-like structures on T cells, or control expression of as yet unidentified cell-surface molecules.

scholarly journals Immunoregulatory circuits among T-cell sets. I. T-helper cells induce other T-cell sets to exert feedback inhibition.

1978 ◽  
Vol 147 (4) ◽  
pp. 1106-1115 ◽  
Author(s):  
D D Eardley ◽  
J Hugenberger ◽  
L McVay-Boudreau ◽  
F W Shen ◽  
R K Gershon ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Feedback Inhibition ◽  
Suppressive Activity ◽  
T Helper ◽  
Suppressor Activity ◽  
Surface Phenotype ◽  
Helper Activity ◽  
And Function

These experiments test the hypothesis that cells carrying the Ly1+23- surface phenotype are programmed exclusively for helper and not suppressive activity regardless of external conditions such as the mode or type of antigen stimulation. To this end, we have stimulated purified populations of Ly1 cells with antigen in vitro using conditions devised to induce unselected T cells to express optimal levels of antigen specific T-suppressor activity. We find that after such stimulation, Ly1 cells generate SRBC-specific T-helper activity but not T-suppressive activity. These findings establish that the Ly1.2+,2.2/3.2- surface phenotype is a stable, and probably invariant, marker of T cells that are programmed to express only helper activity and have lost the capacity to directly suppress the antibody response. These findings support the concept that the genetic program for a single differentiated set of cells combines information for cell surface phenotype and function. We also demonstrate that antigen-stimulated Ly1 cells, in addition to inducing B cells to secrete antibody, can induce or activate other sets of resting T cells to develop profound suppressive effects. The surface phenotype of this feedback suppressive T-cell set is shown to be: Ly1+2+3+Qa1+. These findings, taken together, indicate that activation of resting Ly123 cells by immune Ly1 TH cells may represent an important homeostatic immunoregulatory mechanism.

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