scholarly journals Induction of human IgE synthesis requires interleukin 4 and T/B cell interactions involving the T cell receptor/CD3 complex and MHC class II antigens.

1989 ◽  
Vol 169 (4) ◽  
pp. 1295-1307 ◽  
Author(s):  
D Vercelli ◽  
H H Jabara ◽  
K Arai ◽  
R S Geha
Keyword(s):  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Cell Interaction ◽  
Class Ii ◽  
Ige Synthesis ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigens

The induction of IgE synthesis by IL-4 requires T cells and monocytes, as well as T cell- and monocyte-derived cytokines. Optimal cytokine combinations, however, fail to induce highly purified B cells to secrete IgE, indicating that additional signals are required. We show herein that the induction of human IgE synthesis by rIL-4 requires cognate interaction between the T cell receptor/CD3 complex on T cells and MHC class II antigens on B cells: mAbs directed against these molecules completely blocked IL-4-dependent IgE induction. mAbs against cell adhesion molecules (CD2, CD4, LFA-1) also inhibited IgE synthesis induced by IL-4, confirming that cell-cell contact is necessary for IgE induction. The requirement for cognate T/B cell interaction was further shown by comparing the IgE-inducing ability of two human IL-4-producing alloreactive T cell clones: F6, which recognizes MHC class II antigens on both B cells and monocytes, and A1, which recognizes an HLA-DP-associated epitope expressed on monocytes, but not on B cells. When incubated with B cells and monocytes from a normal donor bearing the appropriate alloantigen, clone F6, but not clone A1, induced vigorous IgE synthesis, although both clones proliferated and secreted IL-4. Taken together, our results suggest that at least two, possibly synergizing, signals are required for the T cell-dependent induction of IgE synthesis by B cells: one signal is delivered by cognate T/B cell interaction, the other by T cell-derived IL-4.

scholarly journals Two levels of help for B cell alloantibody production.

1996 ◽  
Vol 183 (2) ◽  
pp. 699-703 ◽  
Author(s):  
D J Steele ◽  
T M Laufer ◽  
S T Smiley ◽  
Y Ando ◽  
M J Grusby ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Igg Antibodies ◽  
Cd4 Cells ◽  
Mhc Class Ii Antigens ◽  
Cd4 Cell ◽  
Class Ii Antigens ◽  
Deficient Mice

We have examined whether T cell stimulation by direct or indirect pathways contributes to alloantibody production by B cells after major histocompatibility complex (MHC)-disparate skin graft rejection in mice. Experiments were performed using normal mice, MHC class II-deficient mice, MHC class II-deficient mice with an intact peripheral CD4+ cell population (due to expression of class II antigens only on thymic epithelium), mice lacking the cytoplasmic tail of their MHC class II antigens, and mice depleted of CD4+ cells by anti-CD4 monoclonal antibody treatment. Depletion of recipient CD4+ cells reduced alloantibody production to barely detectable levels. Absence of donor MHC class II antigens did not affect the production of either immunoglobulin (Ig)M or IgG antibodies directed at class I alloantigens. Absence of recipient MHC class II antigens, however, led to production of only IgM but not IgG antibodies, even if the recipients had an intact CD4+ cell population. Absence of the cytoplasmic tail of the recipient's MHC class II antigens led to the production of slightly reduced amounts of IgG antibody. These findings indicate that (a) CD4+ cells are essential helper cells for B cell alloantibody production; (b) production of IgM alloantibody can occur with help from CD4+ cells, which recognize either donor class II antigens or modified recipient class II antigens; (c) isotype switching from IgM to IgG alloantibody requires help from CD4+ cells activated by antigens presented by recipient MHC class II molecules; and (d) the cytoplasmic domain of the recipient MHC class II molecules may be involved in the mechanism that leads to isotype switching by B cells. Thus, there are two levels of CD4-mediated help available for B cells responding to alloantigens: one (involving a noncognate interaction) can produce B cell activation, and a second (involving a cognate interaction) is required for differentiation and IgG alloantibody production.

Recognition of MHC Class II Antigens by the CD4: T Cell Receptor Complex

H-2 Antigens ◽  
1987 ◽  
pp. 441-449
Author(s):  
Charles A. Janeway ◽  
Pilar Portoles ◽  
John P. Tite ◽  
Jose Rojo ◽  
Kaj Saizawa ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii ◽  
Cd4 T Cell ◽  
Receptor Complex ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigens

Expression of Lymphocyte Activation Gene 3 (LAG-3/CD223) by Chronic Lymphocytic Leukemia B Cells.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2952-2952
Author(s):  
Han-Yu Chuang ◽  
Yu-Tsueng Liu ◽  
Laura Z. Rassenti ◽  
Lang Huynh ◽  
Dennis Carson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Flow Cytometry ◽  
T Cell ◽  
B Cells ◽  
Chronic Lymphocytic Leukemia ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Lymphocytic Leukemia ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigens

Abstract The clinical course of chronic lymphocytic leukemia (CLL) is variable. DNA-microarray studies have shown that the gene-expression patterns of CLL cells with unmutated IgVH genes are similar to those of cells with mutated IgVH genes, but that the patterns of both are distinct from those of other leukemias and lymphomas. Nevertheless, the two subtypes of CLL can be distinguished by the differential expression of a small number of genes, one of which encodes ZAP-70, an intracellular tyrosine kinase with a critical role in T-cell receptor signaling. Further analysis of the mutation status of IgVH genes and ZAP-70 expression revealed that CLL patients with B cells expressing ZAP-70 and unmutated IgVH genes had a more aggressive disease. LAG-3 (CD223) is thought to play a role in immune responses mediated by T and NK cells. LAG-3, a CD4 homolog, is a ligand for MHC class II antigens. Similar to ZAP-70, LAG-3 is selectively expressed on activated T and NK cells and has recently been shown to be expressed on T-cell activated B cells. We compared the gene expression profiles of the B cells purified from 15 CLL patients using the Affymetrix HG-U133 plus 2.0. This analysis revealed LAG-3 and parathymosin differentially expressed at higher levels by the CLL cells expressing ZAP-70 and unmutated IgVH genes. LAG-3 and parathymosin are located on chromosome 12p13 with head-to-tail orientation. To examine for surface expression of LAG-3, we performed flow cytometry on these same 15 CLL samples using an anti LAG-3 mAb (CD223). We found LAG-3 expressed at high levels by the CD5/CD19 B cells of 4/8 (50%) cases that expressed ZAP-70 and unmutated IgVH genes. Conversely, the samples with B cells lacking ZAP-70 and with mutated IgVH genes did not express LAG-3 (0/7). All samples (15/15) expressed high level of MHC class II antigens, as assessed by flow cytometry. LAG-3 may interact with MHC class II molecules expressed by CLL cells to form an autocrine loop that may further enhance the activation of ZAP-70-expressing CLL B cells. Further analysis is needed to delineate the role of LAG-3 in the pathogenesis and/or progression of this disease.

The role of N-linked oligosaccharides of MHC class II antigens in T cell stimulation

1994 ◽  
Vol 172 (1) ◽  
pp. 95-104 ◽  
Author(s):  
Bishwajit Nag ◽  
H. Garrett Wada ◽  
Subhashini Arimilli ◽  
Katherine Fok ◽  
David Passmore ◽  
...  
Keyword(s):  
T Cell ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Cell Stimulation ◽  
T Cell Stimulation ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigens

Immunohistochemical analysis of human MHC class II antigens in B-cell non-Hodgkin's lymphomas

1985 ◽  
Vol 145 (2) ◽  
pp. 185-194 ◽  
Author(s):  
A. S. Krajewski ◽  
K. Guy ◽  
A. E. Dewar ◽  
D. Cossar
Keyword(s):  
B Cell ◽  
Mhc Class Ii ◽  
Immunohistochemical Analysis ◽  
Class Ii ◽  
Mhc Class Ii Antigens ◽  
Hodgkin's Lymphomas ◽  
Class Ii Antigens

scholarly journals Helper T cell-dependent human B cell differentiation mediated by a mycoplasmal superantigen bridge.

1990 ◽  
Vol 171 (6) ◽  
pp. 2153-2158 ◽  
Author(s):  
J R Tumang ◽  
D N Posnett ◽  
B C Cole ◽  
M K Crow ◽  
S M Friedman
Keyword(s):  
B Cells ◽  
B Cell ◽  
Mhc Class Ii ◽  
Cell Activation ◽  
Cell Interaction ◽  
Class Ii ◽  
B Cell Differentiation ◽  
Th Cells ◽  
Human B Cells ◽  
Th Cell

Experimentally induced murine graft-vs.-host disease may be characterized by hypergammaglobulinemia, autoantibody formation, and immune complex-mediated organ system damage that mimics SLE. These autoimmune phenomena are mediated by abnormal Th-B cell cooperation, across MHC disparities, in which donor-derived allospecific Th cells recognize and interact with MHC class II antigens on the surface of recipient B cells. Microbial toxins, termed superantigens, which bind to MHC class II molecules and activate selected T cells based on TCR variable gene usage, may induce a similar form of Th-B cell interaction. In the present study, we generated and characterized human Th cell lines reactive with the Mycoplasma arthritidis superantigen (MAM). The essential observation is that resting human B cells bind MAM and present it to superantigen-reactive autologous or allogeneic Th cells, resulting in both Th cell activation and a consequent polyclonal Ig response by the superantigen-bearing B cells.

A role for MHC Class II antigens in B-cell activation

1989 ◽  
Vol 2 ◽  
pp. 215-223 ◽  
Author(s):  
Nuala Mooney ◽  
Catherine Grillot-Courvalin ◽  
Claire Hivroz ◽  
Dominique Charron
Keyword(s):  
B Cell ◽  
Mhc Class Ii ◽  
Cell Activation ◽  
Class Ii ◽  
B Cell Activation ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigens

scholarly journals The staphylococcal toxic shock syndrome toxin 1 triggers B cell proliferation and differentiation via major histocompatibility complex-unrestricted cognate T/B cell interaction.

1989 ◽  
Vol 170 (6) ◽  
pp. 2011-2022 ◽  
Author(s):  
W Mourad ◽  
P Scholl ◽  
A Diaz ◽  
R Geha ◽  
T Chatila
Keyword(s):  
Cell Proliferation ◽  
B Cells ◽  
B Cell ◽  
Mhc Class Ii ◽  
Cell Interaction ◽  
Class Ii ◽  
Toxic Shock ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Toxic Shock Syndrome Toxin

The Staphylococcus aureus exotoxin toxic shock syndrome toxin 1 (TSST-1) is a potent activator of T cells and monocytes. We have recently demonstrated that TSST-1 is a superantigen that binds monomorphic determinants on MHC class II molecules. In the present study, we have examined the effect of TSST-1 on the activation and differentiation of high density human tonsillar B cells. TSST-1 bound to tonsilar B cells with high affinity and saturation kinetics. This binding was effectively inhibited by a combination of anti-HLA-DR and anti-HLA-DQ mAbs. Treatment of purified B cells with TSST-1 failed to induce B cell proliferation or Ig production. However, in the presence of irradiated T cells, TSST-1 induced resting B cells to proliferate and differentiate into Ig secretory cells. TSST-1 mimicked nominal antigen in that its induction of B cell responses was strictly dependent on physical contact between T and B cells, and was profoundly inhibited by anti-MHC class II mAbs, anti-CD3 mAbs, and, to a lesser extent, by anti-CD18 mAbs. However, unlike nominal antigen, TSST-1-mediated T/B cell interactions were MHC unrestricted. These results suggest that TSST-1 induces T cell-dependent B cell proliferation and differentiation by virtue of its ability to mediate MHC-unrestricted cognate T/B cell interaction via the TCR/CD3 complex and MHC class II antigens.

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