About High School Biology About Immunology Applications in Immunomodulation 5

For these two types of immunity you must first understand that they function differently. Autoimmune immunity is much longer than passive immunity, but it takes a certain amount of time from injection to the production of antibodies, just like vaccination. Passive immunity, on the other hand, is mainly used for ** or emergency prevention because it is not produced by the human body itself, just like injecting snake venom.

Innate immunity and adaptive immunity are complementary and inseparable. Innate immunity is often a prerequisite for adaptive immunity, as dendritic cells and phagocytic cells engulf pathogenic organisms is actually a process of processing and presenting antigens, which prepares the conditions for the recognition of adaptive immune responses. Effector molecules of adaptive immune responses can greatly promote innate immune responses, such as antibodies that can promote the phagocytic ability of phagocytic cells, called opsonophagocytosis, or promote the cytotoxic effect of NK cells; As another example, many cytokines secreted by T cells promote the maturation, migration, and killing of cells involved in the innate immune response.

Without the involvement of innate immune cells and molecules, there would be no effective specific immune response. Innate immunity and adaptive immunity are two inseparable aspects of the immune system.

1 Structural and functional relevance of cells and molecules involved in innate and adaptive immunity.

1) Immune cells: There are immune cells with both characteristics between cells involved in innate immunity (ME, NK cells) and adaptive immunity (T and B lymphocytes), such as the aforementioned innate lymphocytes NKT, 78T and B1 cells.

2) Immune receptors and immune molecules: There are MHCI and quasi-classical molecules that present antigenic peptides for T cells to recognize, and there are also non-classical MHC molecules and CDLs that act as ligands or present antigens for NK cells and NKT cells to recognize. Figures 1-17 show that the three-dimensional configurations of the three are very similar, and all of them are composed of b lamellar sums.

Helical antigen-binding grooves, some of which also bind to B2 microglobulin.

3) Innate immunity and adaptive immunity carry out cell signaling with similar principles, pathways, and signaling molecules.

The antibody attaches to the surface of the cell membrane and reacts with the antigen is not the root cause of the allergy, but the reason why the manifestations of the allergy manifest themselves. The root cause is because of the loss of control of specific immunity.

The most common symptom of an allergic reaction is a rash.

The reason for this is that histamine alters the permeability of the cell membrane, leading to local edema.

This is my own note, taken with my phone, click to see a larger image, the words in blue parentheses are secreted interleukin.

Among them, the role of helper T cells: recognition, secretion of lymphokines.

Cytotoxic T lymphocytes: recognition, proliferation, differentiation – effector cytotoxic T cells or memory cytotoxic T cells effector cytotoxic T cells: recognize, bind to target cells, and enable them to lyse memory cytotoxic T cells:

Recognition, rapid proliferation and differentiation – effector cytotoxic T cells B lymphocytes: Recognition – sensitized B cells – (interleukin-2) – proliferation and differentiation into effector B cells or memory B cells.

Effector B lymphocytes: produce antibodies.

Memory B lymphocytes: Identification, rapid proliferation and differentiation should be B cells This is what I typed, I hope it can help you.

Take a good look at the detailed process on the book.

1. Humoral immunity is divided into three stages.

1. Induction stage.

Antigen - phagocytic cell - T cell - B cell.

Antigen – B cells.

2. Reaction stage.

B cells – effector B cells.

B cells – memory cells.

3. Effect stage.

Effector B cells – antibodies – antibody binding to antigen – cell grouping or precipitation – phagocytic cell digestion.

2. Cellular immunity.

1. Induction stage.

Antigen – phagocytic cell – T cell.

2. Reaction stage.

T cells – effector T cells.

T cells – memory cells.

3. Effect stage.

Effector T Cells - Target Cells - Target Cell Lysis - Antigens - Antibodies in Body Fluids Eliminate Effector T Cells - Lymphokines

Viruses have to stay in the host cell, generally, otherwise how to multiply.

1Humoral immunity and cellular immunity can be performed at the same time. 2. Humoral immunity does not disappear if the human body is infected with HIV. 3 In fact, both are to be used.

In humoral immunity, when an antigen enters the human body, some of it can be directly recognized by lymphocytic B cells, while others are first contacted by phagocytic cells and analyzed by the epitope on the antigen, and then presented to T cells, where they are presented to B cells, so that B cells differentiate into effector B cells, produce antibodies, and destroy antigens. In humoral immunity, T cells secrete lymphokines to enhance the activity of effector B cells.

In cellular immunity, when the antigen has entered the cells of the human body, the antibody cannot play a role, and the T cells need to differentiate into effector T cells to cause the target cells to lyse and release the antigen into the internal environment, which is destroyed by the antibody.

But the book says that humoral immunity doesn't use T cells, so you'd better follow the book.

4 Effector T cells are differentiated from T cells. 5B cells and T cells.

At the same time, no, humoral immunity is not needed, T cells generate effector T cells, immune cells.

The others they answered, on the second question, theoretically AIDS only destroys T cells, humoral immunity will be retained, but in practice it turns out that AIDS patients eventually lose their immunity completely, as for why, the teacher said that high school does not require it, he does not know. Whining.