Physiological barriers such as skin, mucous membranes, placenta, etc. resist parasite invasion

Phage cells, eosinophils, natural killer lymphocytes and complement in the blood and tissues play a killing role in invading insects

It has immune memory function, and can produce a more rapid and strong immune response when the same parasite is reinfected.

Self-limiting: the gradual elimination of antigens causes the loss of lymphocyte activation conditions and/or enhances the immune regulatory function, and weakens the level of immune response; the failure of parasites to be cleared or negative immune regulation is not established, which can lead to pathological consequences

Eliminating immunity: The host clears the parasites in the body and is completely resistant to reinfection, such as skin leishmaniasis caused by tropical Leishmaniae (rare)

Non-elimination immunity: induces the host to have some immunity to reinfection, but cannot completely remove parasites in the body, such as malaria's worm-bearing immunity and schistosomia's accompanying immunity

By killing parasites, it can protect the host to varying degrees to prevent it from

Excessively strong immune response may lead to pathological damage to host tissue cells, and both results often occur at the same time.

Epimembrane antigen

Body antigen

Egg antigen

Excretion/secretion of antigens

Antigens at different stages

Protein antigen

Polysaccharide antigen

Glycoprotein antigen

Glycolipid antigen

Direct contact with the host, induces protective immune response and/or immunopathological response, and can be used as an immunodiagnostic testing object

Parasite antigens are uptaken by antigen-presenting cells such as macrophages, dendritic cells, and B cells.

Protein antigen is processed into peptides in cells, linked to the main histocompatible complex molecules to form a polypeptide/MHC complex, and is expressed on the cell surface for antigen presentation.

Parasite non-protein antigens can crosslink with B cell surface membrane immunoglobulins, causing B cell activation without T-cell assistance to produce humoral immune effects

Activation, proliferation and differentiation of antigen-specific lymphocytes after recognition of antigens

T cells proliferate and differentiate into sensitized T cells, B cells proliferate and differentiate into plasma cells, and partially form memory cells

Activated antigen presenting cells and T cells produce multiple cytokines to regulate lymphocyte proliferation and differentiation

Interleukin-2 is an important interstitial essential for T cell survival and proliferation

T/B cells recognize specific antigens to produce the first signal that is activated, and provide the second signal, namely the costimulation signal, with the antigen presenting molecule on the cell surface.

Negative regulation: PD-1 receptors on the surface of T cells bind to their ligands to inhibit

Cellular immunity

Humoral immunity

Parasites are parasitic in host cells or cavity, and their unique physiological barriers are isolated from the immune system, such as malaria parasites that are parasitic in red blood cells.

Parasites form protective cyst walls in the host and are isolated from immune cells, such as the cysts of Toxoplasma gondii

Antigen mutation: Parasites have specific antigens at different development stages, and antigens can also be changed at the same development stage, such as Trypanosoma brucea

Molecular simulation and camouflage: The body surface of the parasite expresses similar components to the host tissue, or combines the host component to form antigenic camouflage, such as schistosomiasis lung stage

The surface membrane falls off and update: The worm's surface membrane keeps falling off and renewing, causing the bound antibodies to fall off.

Depletion of specific B cell clones: Parasitic infection induces host polyclonal B cell activation, producing a large number of unprotective antibodies, resulting in specific B cell depletion

Induction and activation of Treg cells: Treg cells inhibit the proliferation, differentiation and effects of immune-active cells, such as mice infected with Schistosoma dysfunction

Insect-derived lymphocytosis factors: Parasite secretions and excretions are lymphocytosis or inhibit lymphocyte activation, such as the thermally stable glycoprotein of Schistosoma mannello and the protease secreted by Trypanosoma cruzi

Production of blocking antibodies: No insecticidal antibodies bound to the surface of the insect block the binding of insecticidal antibodies, such as hosts infected with Schistosoma mannellosa, filaria and trichinidella

Parasite antigens stimulate the host to produce IgE, which binds to mast cells or basophil surface receptors to sensitize

Re-contacting the same antigen occurs, a bridge reaction occurs, the cells are degranulated, and the inflammatory mediators are released, leading to capillary dilation, enhanced permeability, smooth muscle contraction and local inflammation, which can cause allergic shock

The antibodies that cause type I hypersensitivity are mainly IgE, and some IgG subclasses can also mediate

Target cell surface antigens bind to IgG or IgM, resulting in complement activation or damage to target cells through antibody-dependent cell-mediated cytotoxicity

Such as nigra and malaria, insect antigens adsorb on the surface of red blood cells, causing hemolysis and anemia

Parasite antigens form immune complexes with antibodies, which are deposited in tissues to activate complement, leading to inflammatory responses and tissue damage

Schistosoma schistosomiae continuously releases antigens and easily forms immune complexes. The size of the IC determines its clearance rate. IgG type IC is easily cleared, and IgA type is easily deposited.

Systemic pathogenesis is manifested as fever, urticaria, etc., local diseases such as immune complex nephritis

Mediated by T cells, such as the formation of egg granuloma of Schistosoma worm

Parasitic infections can have multiple types of hypersensitivity reactions, such as schistosomiasis

By killing parasites, it can protect the host to varying degrees to prevent it from

Excessively strong immune response may lead to pathological damage to host tissue cells, and both results often occur at the same time.

Parasite antigens are uptaken by antigen-presenting cells such as macrophages, dendritic cells, and B cells.

Protein antigen is processed into peptides in cells, linked to the main histocompatible complex molecules to form a polypeptide/MHC complex, and is expressed on the cell surface for antigen presentation.

Parasite non-protein antigens can crosslink with B cell surface membrane immunoglobulins, causing B cell activation without T-cell assistance to produce humoral immune effects

Activation, proliferation and differentiation of antigen-specific lymphocytes after recognition of antigens

T cells proliferate and differentiate into sensitized T cells, B cells proliferate and differentiate into plasma cells, and partially form memory cells

Activated antigen presenting cells and T cells produce multiple cytokines to regulate lymphocyte proliferation and differentiation

Interleukin-2 is an important interstitial essential for T cell survival and proliferation

T/B cells recognize specific antigens to produce the first signal that is activated, and provide the second signal, namely the costimulation signal, with the antigen presenting molecule on the cell surface.

Negative regulation: PD-1 receptors on the surface of T cells bind to their ligands to inhibit

Cellular immunity

Humoral immunity

Parasite antigens stimulate the host to produce IgE, which binds to mast cells or basophil surface receptors to sensitize

Re-contacting the same antigen occurs, a bridge reaction occurs, the cells are degranulated, and the inflammatory mediators are released, leading to capillary dilation, enhanced permeability, smooth muscle contraction and local inflammation, which can cause allergic shock

The antibodies that cause type I hypersensitivity are mainly IgE, and some IgG subclasses can also mediate

Target cell surface antigens bind to IgG or IgM, resulting in complement activation or damage to target cells through antibody-dependent cell-mediated cytotoxicity

Such as nigra and malaria, insect antigens adsorb on the surface of red blood cells, causing hemolysis and anemia

Parasite antigens form immune complexes with antibodies, which are deposited in tissues to activate complement, leading to inflammatory responses and tissue damage

Schistosoma schistosomiae continuously releases antigens and easily forms immune complexes. The size of the IC determines its clearance rate. IgG type IC is easily cleared, and IgA type is easily deposited.

Systemic pathogenesis is manifested as fever, urticaria, etc., local diseases such as immune complex nephritis

Mediated by T cells, such as the formation of egg granuloma of Schistosoma worm

Parasitic infections can have multiple types of hypersensitivity reactions, such as schistosomiasis