Interactions between immune cells during antibody formation
Interactions between immune cells during antibody formation In the course of antibody production, the response to TD antigen has been proven to be the result of the interaction between Mφ, T-line cells, and B-line cells. Then, whether Mφ directly presents antigen is T cells or B cells? Or both? Based on the analysis of existing data, they may have the interaction between Mφ and T, the interaction between T and B, and the interaction between Mφ and B cells.
1. The interaction between macrophages and TH cells
TH cells must be activated from TH at rest to be activated to help B cells produce antibodies. Regarding the mechanism of TH cell activation, a dual-signal hypothesis was proposed based on existing experimental data.
Recent experiments have shown that at least two molecules on the surface of antigen presenting cells (APC) are related to the activation of TH cells. One is an antigen presentation molecule, which is composed of MHC molecules, which can be combined with exogenous or endogenous antigen peptide fragments, and then transported to the cell surface and presented to T cells, which generates the first activation signal by TCR / CE3 stimulation . Another kind of molecule is the so-called costimulating molecules (CM), which is composed of a group of adhesion molecules. It not only promotes direct contact between APC and T cells, but also has the function of inducing signal transmission. This group of molecules can be combined with costimulatory molecule receptors (CMR) on T cells to stimulate them to produce costimulatory signals, the so-called second signal.
The CMR or accessory molecules on T cells are also composed of a group of adhesion molecules (Table 11-7). The molecular structure and function of CMR and its ligands and signal transduction pathways need to be further studied, but the CD28 molecule and CTLA-4 molecule and its ligand B7 / BB1 molecule are considered to be the main molecules that produce co-stimulatory signals (Figure 11-2).
Under these two signals, T cells can be activated to synthesize and secrete IL-2 and express IL-2R, which ultimately leads to cell division and clonal expansion. If there is no second signal, T cells are not activated nor cause clonal expansion, and are in a clonal aneergy state (Figure 11-3).
Thymus cell CD58 (LFA-3) + + CD4 55kD monomer Ig CD4 + T cell MHC II molecule + + CD8 78kD monomer Ig CD8 + T cell MHC II molecule + + CD11a / CD18
(LFA-1) 180 / 95kD diadhesin bone marrow-derived cells CD54 (ICAM-1)? + CD28 90kD homodimer CD4 +
CD8 + T (50%) B7 / BB1 + + CDw49 / CD29
(VLA-4, 5, 6) Heterodimeric Adhesin Leukocytes
Other cells Extracellular matrix VCAM-1 + + gP39 (CD40L) CD4 + T cells CD40
Blocking or giving the second signal can artificially modulate the immune response to enhance or suppress it, providing a new means for immunotherapy. For example, blocking the generation of the second signal can make T cells in an immune tolerance state and reduce the body's immune response, which is beneficial to prevent the occurrence of transplant rejection and the treatment of hypersensitivity diseases and autoimmune diseases. If the B7 gene is introduced into certain tumor cells, it can enhance the body's anti-tumor immune response. At present, there have been many reports of experimental studies in this area (Figure 11-4).
2. The interaction between TH cells and B cells
(1) B cell response to T cell dependent antigen
Interactions between immune cells during antibody formation Generally, when a large amount of antigen enters the unimmunized body, the antigen-presenting cells are mostly completed by macrophages when the initial immune response is induced. After activation of TH cells by Mφ, the activated TH cells help B cells to produce antibodies and form memory B cells. But when another immune response occurs, the antigen-presenting cells are mainly undertaken by the expanded B-cell clones. Because of its increased affinity for membrane Ig receptors, it can also take up a small amount of antigen, so it can replace the antigen presentation of macrophages.
In the past, it was thought that the interaction between B cells and TH cells was brought into contact through the bridging of antigens, that is, the antigen receptor of B cells could recognize the hapten part of the antigen molecule, while the antigen receptor of TH cells could recognize the antigen The carrier part of the molecule. However, experiments in recent years have proved that B cells are the same as Mφ and also interact with TH cells through antigen presentation. That is, B cells can bind to the antigen through their membrane Ig receptor protein, namely T-dependent antigen, and take up the antigen through internalization. After processing, the T cell determinants are combined with MHC class II molecules to form an MHC-peptide molecular complex and transported to the surface of B cells to present it to TH cells, so the interaction between B cells and TH cells is also MHC restricted Sexual.
Interaction between immune cells during antibody formation B cells and TH cells can directly contact each other through their adhesion molecules and antigen presentation, and can induce each other to activate them. Activated B cells With the help of TH cells, B cells eventually proliferate and differentiate into plasma cells that synthesize and secrete various immunoglobulin molecules.
B cells can stimulate the T cell antigen receptor (TCR / CD3) to generate activation signal 1 through its antigen presentation, and through its surface B7 and other co-stimulatory molecules and corresponding receptor molecules on the surface of T cells such as CD28, IFA-1, etc. Combined, it can stimulate the generation of a co-stimulatory signal (ie signal 2), which can activate TH cells under the action of dual signals.
B cells bind to antigens through their BCR, the surface Ig receptor, and the Iga and Igβ chains are equivalent to CD3 molecules and can transmit activation signals1. In recent years, it has been proved that the CD40 molecule expressed on the surface of B cells can bind to the corresponding ligand molecule gP39 (ie, CD40 ligand molecule, CD40L) on the surface of T cells to stimulate it to generate activation signal 2, which can activate B cells under the action of this dual signal (Figure 11-5).
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